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  • 1.
    Abrahams, M
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Anestesiologi.
    Eriksson, H
    Björnström, Karin
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Östergötlands Läns Landsting, MKC - Medicin och kirurgicentrum, Anestesi.
    Eintrei, Christina
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Östergötlands Läns Landsting, MKC - Medicin och kirurgicentrum, Anestesi.
    Effects of propofol on extracellular acidification rates in primary cortical cell cultures: application of silicon microphysiometry to anaesthesia.1999Ingår i: British Journal of Anaesthesia, ISSN 0007-0912, E-ISSN 1471-6771, Vol. 83, s. 567-569Artikel i tidskrift (Refereegranskat)
  • 2.
    Andersson, Henrik
    et al.
    Linköpings universitet, Medicinska fakulteten. Östergötlands Läns Landsting, Sinnescentrum, Anestesi- och intensivvårdskliniken US. Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning.
    Björnström-Karlsson, Karin
    Region Östergötland, Sinnescentrum, Anestesi- och intensivvårdskliniken US. Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning. Linköpings universitet, Medicinska fakulteten.
    Eintrei, Christina
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Sinnescentrum, Anestesi- och intensivvårdskliniken US.
    Sundqvist, Tommy
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Medicinska fakulteten.
    Orexin A Phosphorylates the gamma-Aminobutyric Acid Type A Receptor beta(2) Subunit on a Serine Residue and Changes the Surface Expression of the Receptor in SH-SY5Y Cells Exposed to Propofol2015Ingår i: Journal of Neuroscience Research, ISSN 0360-4012, E-ISSN 1097-4547, Vol. 93, nr 11, s. 1748-1755Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Propofol activates the gamma-aminobutyric acid type A receptor (GABA(A)R) and causes a reversible neurite retraction, leaving a thin, thread-like structure behind; it also reverses the transport of vesicles in rat cortical neurons. The awakening peptide orexin A (OA) inhibits this retraction via phospholipase D (PLD) and protein kinase CE (PKCE). The human SH-SY5Y cells express both GABA(A)Rs and orexin 1 and 2 receptors. These cells are used to examine the interaction between OA and the GABAAR. The effects of OA are studied with flow cytometry and immunoblotting. This study shows that OA stimulates phosphorylation on the serine residues of the GABA(A)R beta(2) subunit and that the phosphorylation is caused by the activation of PLD and PKCE. OA administration followed by propofol reduces the cell surface expression of the GABA(A)R, whereas propofol stimulation before OA increases the surface expression. The GABA(A)R beta(2) subunit is important for receptor recirculation, and the effect of OA on propofol-stimulated cells may be due to a disturbed recirculation of the GABA(A)R. (C) 2015 Wiley Periodicals, Inc.

  • 3.
    Bergdahl, Björn
    et al.
    Linköpings universitet, Hälsouniversitetet.
    Eintrei, Christina
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa.
    Fyrenius, Anna
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa.
    Hultman, Per
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin.
    Ledin, Torbjörn
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neurovetenskap.
    Theodorsson, Elvar
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin.
    In the Forefront of Development:The New Undergraduate Medical Curriculu2006Ingår i: Celebrating the Past by Expanding the Future: The Faculty of Health Science, Linköping University 1986–2006 / [ed] Mats Hammar, Björn Bergdahl, Lena Öhman, Linköping: Linköping University Electronic Press, 2006, 1, s. 98-102Kapitel i bok, del av antologi (Övrigt vetenskapligt)
  • 4.
    Bergdahl, Björn
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård. Östergötlands Läns Landsting, Hjärtcentrum, Kardiologiska kliniken.
    Eintrei, Christina
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Östergötlands Läns Landsting, Anestesi- och operationscentrum, Intensivvårdskliniken US.
    Fyrenius, Anna
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Klinisk fysiologi.
    Hultman, Per
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Molekylär och immunologisk patologi. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk patologi och klinisk genetik.
    Theodorsson, Elvar
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för biomedicin och kirurgi, Avdelningen för klinisk kemi. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk kemi.
    Läkarutbildningen i Linköpings förnyas. Problembaserat lärande, basvetenskap och folkhälsa förstärks2005Ingår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 102, nr 38, s. 2654-2658Artikel i tidskrift (Övrigt vetenskapligt)
  • 5.
    Björnström, Karin
    et al.
    Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Linköpings universitet, Institutionen för medicin och vård, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    Eintrei, Christina
    Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Linköpings universitet, Institutionen för medicin och vård, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    The difference between sleep and anaesthesia is in the intracellular signal: propofol and GABA use different subtypes of the GABAA receptor β subunit and vary in their interaction with actin2003Ingår i: Acta Anaesthesiologica Scandinavica, ISSN 0001-5172, E-ISSN 1399-6576, Vol. 47, nr 2, s. 157-164Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Propofol is known to interact with the γ-aminobutyric acidA (GABAA) receptor, however, activating the receptor alone is not sufficient for producing anaesthesia.

    Methods: To compare propofol and GABA, their interaction with the GABAA receptor β subunit and actin were studied in three cellular fractions of cultured rat neurons using Western blot technique.

    Results: Propofol tyrosine phosphorylated the GABAA receptor β2 (MW 54 and 56 kDa) and β3 (MW 57 kDa) subtypes. The increase was shown in both the cytoskeleton (β2(54) and β2(56) subtypes) and the cell membrane (β2(54) and β3 subtypes). Concurrently the 56 kDa β2 subtype was reduced in the cytosol. Propofol, but not GABA, also tyrosine phosphorylated actin in the cell membrane and cytoskeletal fraction. Without extracellular calcium available, the amount of actin decreased in the cytoskeleton, but tyrosine phosphorylation was unchanged. GABA caused increased tyrosine phosphorylation of β2(56) and β3 subtypes in the membrane and both β2 subtypes in the cytoskeleton but no cytosolic tyrosine phosphorylation.

    Conclusion: The difference between propofol and GABA at the GABAA receptor was shown to take place in the membrane, where the β2(54) was increased by propofol and instead the β2(56) subtype was increased by GABA. Only propofol also tyrosine phosphorylated actin in the cell membrane and cytoskeletal fraction. This interaction between the GABAA receptor and actin might explain the difference between anaesthesia and physiological neuronal inhibition.

  • 6.
    Björnström, Karin
    et al.
    Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Linköpings universitet, Institutionen för medicin och vård, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    Eintrei, Christina
    Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Linköpings universitet, Institutionen för medicin och vård, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    Volatile anesthetics cause changes in intracellular calcium, tyrosine phosphorylation and actin morphologyManuskript (preprint) (Övrigt vetenskapligt)
    Abstract [en]

    Background: The cellular effects of anesthetics is poorly known. The GABAA receptor has been suggested as the main target for most anesthetics. In previous studies we have shown that propofol tyresine phosphorylates the GABAA receptor ß subunit, increases intracellular calcium and changes the actin morphology of neurons.

    Aim: To investigate the effects of the volatile anesthetics sevoflurane, isoflurane and nitmus oxide on changes in [Ca2+]i tyrosine phosphorylation and actin morphology in cultured rat neurons.

    Methods: Western blotting (WB) was used to visualize tyrosine phosphorylated proteins. Fluorescence microscopy after rhodamine-phalloidin labelling of actin was used to calculate the number of actin ring structures eaused by sevoflurane. Intracellular calcium was measured with the calcium-binding probe Fura-2 on single cells.

    Results: A protein of approx. 60 kDa increased dose-dependently in tyresine phosphorylation by sevoflurane in the membrane and cytoskeletal fractions, and was simultaneausly reduced in the cytosol. Isoflurane instead increased the tyresine phosphorylation of the same protein in the cytosol with only a slight increase in the membrane and no changes in the cytoskeletal fraction. Nitrous oxide did not cause any changes campared to air in the cytosol and was not detectable in the membrane. However, in the cytoskeletal fraction, the increase in tyrosine phosphorylation was high compared to air. Sevoflurane but not nitrous oxide or air increased the [Ca2+]i· Sevoflurane also eaused actin ring structures with a maximum after 20 minutes.

    Conclusion: Sevoflurane, isoflurane and nitrous oxide all have different signal pathways. The 60 kDa protein is probably the GABAA receptor ß subunit. According to the changes in tyrosine phosphorylation, changes in actin morphology and intracellular calcium, sevoflurane behaves most like the intravenous anesthetic propofol.

  • 7.
    Björnström, Karin
    et al.
    Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Linköpings universitet, Hälsouniversitetet.
    Holmgren, Susanna
    Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Linköpings universitet, Hälsouniversitetet.
    Loverock, A.
    Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Linköpings universitet, Hälsouniversitetet.
    Wijkman, Magnus
    Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Linköpings universitet, Hälsouniversitetet.
    Lindroth, Margareta
    Linköpings universitet, Institutionen för biomedicin och kirurgi, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Eintrei, Christina
    Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Linköpings universitet, Hälsouniversitetet.
    Rho and Rho Kinase are involved in the signal transduction cascade caused by propofolManuskript (preprint) (Övrigt vetenskapligt)
    Abstract [en]

    Background: Propofol is known to interact with the γ-aminobutyric acidA (GABAA) receptor, however, activating the receptor alone is not sufficient for producing anaesthesia. Propofol tyresine phosphorylates the GABAA receptor and reorganises the actin cytoskeleton, eausing ring structures and rnembrane ruffles. Propofol, but not GABA, the endogenous tigand for the GABAA receptor, tyresine phosphorylates actin, both in the membrane and cytoskeletal fractions of the neuron.

    Aim: How does propofol cause the actin reorganisation and is this a specific effect of propofol? Is the small membrane associated G-protein rho involved in the signal cascade towards the actin reorganisation?

    Methods: Westem blotting (WB) was used to visualize tyresine phosphorylated immunoprecipitated proteins and changes in actin between the different cellularcompartments after inhibition with rho (C3 exotoxin) and rho kinase (ROK) (HA-1077) inhibitors. Fluoreseenee mireoscopy after rhodamine-phalloidin labelling of actin was used to calculate the number of actin ring structures caused by propofol or GABA, in same experiments combined with pre-incubation with C3 exotoxin, HA- 1077 or the tyrosine kinase inhibitor Herbimycin A. Propofol-stimulated cells were studied with confocal microscopy.

    Results: Propofol eaused an increased tyresine phosphorylation, that was reduced by C3 exotoxin, of a 160 kDa protein after two minutes stimulation. The 160 kDa protein is still unidentified. The actin ring structures caused by propofol was shown with confocal microscopy to go almost through the entire cell. The amount of rings were reduced by C3 exatoxin as well as HA-1077. Furthermore, w hen a tyrosine kinase bioeker was used no ring structures were formed. However, GABA did not produce any ring structures. When the actin content of the cellular campartments were analysed, C3 exatoxin treated cells showed an increased amount of actin in the cytoskeletal fraction, simultaneausly with a decrease in both the membrane and the cytosol fractions. The ROK bioeker on ly eaused a reduction of actin in the cytosol/membrane fractions, but no increase was observed in the cytoskeleton.

    Conclusion: Propofol, but not GABA, eauses actin ring structures in neurons. Propofol uses the rho and rho kinase pathway to reorganize the actin cytoskeleton into ring structures, which is also dependent on a tyresine klnase. Propofol also eauses an unidentified rho dependent 160 kDa protein to be tyresine phosphorylated. The activation eaused by propofol of rho and rho kinase causes actin to be moved from the cytoskeleton to the cell membrane and cytosol. This reorganisation of actin might influence the GABAA receptor by keeping it open, thus allowing the cell to be hyperpolarized for longer time, and consequently maintain anaesthesia.

  • 8.
    Björnström, Karin
    et al.
    Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Linköpings universitet, Institutionen för medicin och vård, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    Sjölander, Anita
    Division of Experimental Pathology, Lund University, Malmö, Sweden.
    Schippert, Åsa
    Linköpings universitet, Institutionen för biomedicin och kirurgi, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Eintrei, Christina
    Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Linköpings universitet, Institutionen för medicin och vård, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    A tyrosine kinase regulates propofol-induced modulation of the β-subunit of the GABAA receptor and release of intracellular calcium in cortical rat neurones2002Ingår i: Acta Physiologica Scandinavica, ISSN 0001-6772, E-ISSN 1365-201X, Vol. 175, nr 3, s. 227-235Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Propofol, an intravenous anaesthetic, has been shown to interact with the β-subunit of the γ-amino butyric acidA (GABAA) receptor and also to cause changes in [Ca2+]i. The GABAA receptor, a suggested target for anaesthetics, is known to be regulated by kinases. We have investigated if tyrosine kinase is involved in the intracellular signal system used by propofol to cause anaesthesia. We used primary cell cultured neurones from newborn rats, pre-incubated with or without a tyrosine kinase inhibitor before propofol stimulation. The effect of propofol on tyrosine phosphorylation and changes in [Ca2+]i were investigated. Propofol (3 μg mL−1, 16.8 μM) increased intracellular calcium levels by 122 ± 34% (mean ± SEM) when applied to neurones in calcium free medium. This rise in [Ca2+]i was lowered by 68% when the cells were pre-incubated with the tyrosine kinase inhibitor herbimycin A before exposure to propofol (P < 0.05). Propofol caused an increase (33 ± 10%) in tyrosine phosphorylation, with maximum at 120 s, of the β-subunit of the GABAA-receptor. This tyrosine phosphorylation was decreased after pre-treatment with herbimycin A (44 ± 7%, P < 0.05), and was not affected by the absence of exogenous calcium in the medium. Tyrosine kinase participates in the propofol signalling system by inducing the release of calcium from intracellular stores and by modulating the β-subunit of the GABAA-receptor.

  • 9.
    Björnström, Karin
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Östergötlands Läns Landsting, Anestesi- och operationscentrum, Intensivvårdskliniken US.
    Turina, Dean
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård.
    Loverock, A.
    Department of Anaesthesiology Linköping University.
    Lundgren, S.
    Department of Anaesthesiology Linköping University.
    Wijkman, Magnus
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin.
    Lindroth, Margaretha
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Medicinsk mikrobiologi.
    Eintrei, Christina
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Östergötlands Läns Landsting, Anestesi- och operationscentrum, Intensivvårdskliniken US.
    Characterisation of the signal transduction cascade caused by propofol in rat neurons: From the GABAA receptor to the cytoskeleton2008Ingår i: Journal of Physiology and Pharmacology, ISSN 0867-5910, E-ISSN 1899-1505, Vol. 59, nr 3, s. 617-632Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The anaesthetic propofol interacts with the GABAA receptor, but its cellular signalling pathways are not fully understood. Propofol causes reorganisation of the actin cytoskeleton into ring structures in neurons. Is this reorganisation a specific effect of propofol as apposed to GABA, and which cellular pathways are involved? We used fluorescence-marked actin in cultured rat neurons to evaluate the percentage of actin rings caused by propofol or GABA in combination with rho, rho kinase (ROK), PI3-kinase or tyrosine kinase inhibitors, with or without the presence of extracellular calcium. Confocal microscopy was performed on propofol-stimulated cells and changes in actin between cellular compartments were studied with Western blot. Propofol (3 μg·ml-1), but not GABA (5 μM), caused transcellular actin ring formation, that was dependent on influx of extracellular calcium and blocked by rho, ROK, PI3-kinase or tyrosine kinase inhibitors. Propofol uses rho/ROK to translocate actin from the cytoskeleton to the membrane and its actin ring formation is dependent on an interaction site close to the GABA site on the GABAA receptor. GABA does not cause actin rings, implying that this is a specific effect of propofol.

  • 10.
    Björnström-Karlsson, Karin
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Sinnescentrum, Anestesi- och intensivvårdskliniken US.
    Turina, Dean
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning. Linköpings universitet, Hälsouniversitetet.
    Strid, Tobias
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin. Linköpings universitet, Hälsouniversitetet.
    Sundqvist, Tommy
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Hälsouniversitetet.
    Eintrei, Christina
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Sinnescentrum, Anestesi- och intensivvårdskliniken US.
    Orexin A Inhibits Propofol-Induced Neurite Retraction by a Phospholipase D/Protein Kinase C-epsilon-Dependent Mechanism in Neurons2014Ingår i: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 9, nr 5, s. e0097129-Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: The intravenous anaesthetic propofol retracts neurites and reverses the transport of vesicles in rat cortical neurons. Orexin A (OA) is an endogenous neuropeptide regulating wakefulness and may counterbalance anaesthesia. We aim to investigate if OA interacts with anaesthetics by inhibition of the propofol-induced neurite retraction. Methods: In primary cortical cell cultures from newborn rats brains, live cell light microscopy was used to measure neurite retraction after propofol (2 mu M) treatment with or without OA (10 nM) application. The intracellular signalling involved was tested using a protein kinase C (PKC) activator [phorbol 12-myristate 13-acetate (PMA)] and inhibitors of Rho-kinase (HA-1077), phospholipase D (PLD) [5-fluoro-2-indolyl des-chlorohalopemide (FIPI)], PKC (staurosporine), and a PKC epsilon translocation inhibitor peptide. Changes in PKC epsilon Ser(729) phosphorylation were detected with Western blot. Results: The neurite retraction induced by propofol is blocked by Rho-kinase and PMA. OA blocks neurite retraction induced by propofol, and this inhibitory effect could be prevented by FIPI, staurosporine and PKC epsilon translocation inhibitor peptide. OA increases via PLD and propofol decreases PKC epsilon Ser(729) phosphorylation, a crucial step in the activation of PKC epsilon. Conclusions: Rho-kinase is essential for propofol-induced neurite retraction in cortical neuronal cells. Activation of PKC inhibits neurite retraction caused by propofol. OA blocks propofol-induced neurite retraction by a PLD/PKC epsilon-mediated pathway, and PKC epsilon maybe the key enzyme where the wakefulness and anaesthesia signal pathways converge.

  • 11.
    Eintrei, Christina
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Östergötlands Läns Landsting, Anestesi- och operationscentrum, Intensivvårdskliniken US.
    Bergdahl, Björn
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård. Östergötlands Läns Landsting, Hjärtcentrum, Kardiologiska kliniken.
    Fyrenius, Anna
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Klinisk fysiologi.
    Hultman, Per
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Molekylär och immunologisk patologi. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk patologi och klinisk genetik.
    Theodorsson, Elvar
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för biomedicin och kirurgi, Avdelningen för klinisk kemi. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk kemi.
    Revising a medical PBL-curriculum - the Linköping strategy2004Ingår i: Association for Medical Education in Europe,2004, 2004Konferensbidrag (Övrigt vetenskapligt)
  • 12.
    Eintrei, Christina
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Östergötlands Läns Landsting, MKC - Medicin och kirurgicentrum, Anestesi.
    Sokoloff, L
    Smith, C B
    Effects of diazepam and ketamine administred individually or in combination on regional rates of glucose utilization in rat brain.1999Ingår i: British Journal of Anaesthesia, ISSN 0007-0912, E-ISSN 1471-6771, Vol. 82, s. 596-602Artikel i tidskrift (Refereegranskat)
  • 13.
    Gupta, Anil
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Sinnescentrum, Anestesi- och operationkliniken US.
    Bjornsson, A.
    Department Anaesthesiol and Intens Care, Orebro.
    Fredriksson, M.
    Hallböök, Olof
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Kirurgi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Centrum för kirurgi, ortopedi och cancervård, Kirurgiska kliniken i Östergötland.
    Eintrei, Christina
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Sinnescentrum, Intensivvårdskliniken US.
    Reduction in mortality after epidural anaesthesia and analgesia in patients undergoing rectal but not colonic cancer surgery: a retrospective analysis of data from 655 patients in Central Sweden2011Ingår i: British Journal of Anaesthesia, ISSN 0007-0912, E-ISSN 1471-6771, Vol. 107, nr 2, s. 164-170Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background. There is some evidence that epidural analgesia (EDA) reduces tumour recurrence after breast and prostatic cancer surgery. We assessed whether EDA reduces long-term mortality after colorectal cancer surgery. Methods. All patients having colorectal cancer surgery between January 2004 and January 2008 at Linkoping and Orebro were included. Exclusion criteria were: emergency operations, laparoscopic-assisted colorectal resection, and stage 4 cancer. Statistical information was obtained from the Swedish National Register for Deaths. Patients were analysed in two groups: EDA group or patient-controlled analgesia (PCA group) as the primary method of analgesia. Results. A total of 655 patients could be included. All-cause mortality for colorectal cancer (stages 1-3) was 22.7% (colon: 20%, rectal: 26%) after 1-5 yr of surgery. Multivariate regression analysis identified the following statistically significant factors for death after colon cancer (Pless than0.05): age (greater than72 yr) and cancer stage 3 (compared with stage 1). A similar model for rectal cancer found that age (greater than72 yr) and the use of PCA rather than EDA and cancer stages 2 and 3 (compared with stage 1) were associated with a higher risk for death. No significant risk of death was found for colon cancer when comparing EDA with PCA (P=0.23), but a significantly increased risk of death was seen after rectal cancer when PCA was used compared with EDA (P=0.049) [hazards ratio: 0.52 (0.27-1.00)]. Conclusions. We found a reduction in all-cause mortality after rectal but not colon cancer in patients having EDA compared with PCA technique.

  • 14.
    Hammar, Mats
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Obstetrik och gynekologi. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Kvinnokliniken i Linköping.
    Asp, Malin
    Linköpings universitet, Institutionen för medicin och vård.
    Berlin, Gösta
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Transfusionsmedicin. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk immunologi och transfusionsmedicin.
    Dahlström, Ulf
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Kardiologi. Östergötlands Läns Landsting, Hjärtcentrum, Kardiologiska kliniken.
    Eintrei, Christina
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Östergötlands Läns Landsting, Anestesi- och operationscentrum, Intensivvårdskliniken US.
    Ekdahl, Anne
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för nervsystem och rörelseorgan. Östergötlands Läns Landsting, Närsjukvården i centrala Östergötland, Geriatriska kliniken.
    Ledin, Torbjörn
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för nervsystem och rörelseorgan, Oto-Rhino-Laryngologi. Östergötlands Läns Landsting, Rekonstruktionscentrum, Öronkliniken US.
    Maller, Rolf
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Infektionsmedicin. Östergötlands Läns Landsting, Medicincentrum, Infektionskliniken i Östergötland.
    A new program for better clinical supervision of students. A joint project at the Halsouniversitet and county council in Ostergotland2006Ingår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 103, s. 649-654Artikel i tidskrift (Övrigt vetenskapligt)
  • 15.
    Hammar, Mats
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Obstetrik och gynekologi. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Kvinnokliniken i Linköping.
    Asp, Malin
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård.
    Berlin, Gösta
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Transfusionsmedicin. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk immunologi och transfusionsmedicin.
    Dahlström, Ulf
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Kardiologi. Östergötlands Läns Landsting, Hjärtcentrum, Kardiologiska kliniken.
    Eintrei, Christina
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Östergötlands Läns Landsting, Anestesi- och operationscentrum, Intensivvårdskliniken US.
    Ekdahl, Anne
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för nervsystem och rörelseorgan. Östergötlands Läns Landsting, Närsjukvården i centrala Östergötland, Geriatriska kliniken.
    Ledin, Torbjörn
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för nervsystem och rörelseorgan, Oto-Rhino-Laryngologi. Östergötlands Läns Landsting, Rekonstruktionscentrum, Öronkliniken US.
    Maller, Rolf
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Infektionsmedicin. Östergötlands Läns Landsting, Medicincentrum, Infektionskliniken i Östergötland.
    Ny handlingsplan för bättre klinisk handledning av studenter.2006Ingår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 103, s. 649-654Artikel i tidskrift (Övrigt vetenskapligt)
    Abstract [sv]

        

  • 16.
    Kalman, Sigga
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Östergötlands Läns Landsting, Anestesi- och operationscentrum, Anestesi- och intensivvårdskliniken VIN.
    Linderfalk, C
    Wårdell, Karin
    Linköpings universitet, Tekniska högskolan. Linköpings universitet, Institutionen för medicinsk teknik, Biomedicinsk instrumentteknik.
    Eintrei, Christina
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Östergötlands Läns Landsting, Anestesi- och operationscentrum, Intensivvårdskliniken US.
    Lisander, Björn
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Anestesiologi.
    Differential effect on vasodilatation and pain after intradermal capsaicin in humans during decay of intravenous regional anesthesia with mepivacaine1998Ingår i: Regional anesthesia and pain medicine, ISSN 1098-7339, E-ISSN 1532-8651, Vol. 23, nr 4, s. 402-408Artikel i tidskrift (Refereegranskat)
  • 17. Lindfors, Sara
    et al.
    Alexandersson, Kristina
    Eintrei, Christina
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Östergötlands Läns Landsting, Anestesi- och operationscentrum, Intensivvårdskliniken US.
    Gotthard, Ricci
    Nordström, Louise
    Karlsson, Nadine
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för hälsa och samhälle, Socialmedicin och folkhälsovetenskap.
    Stressande faktorer bland disputerade specialistläkare anställda på ett universitetssjukhus2005Rapport (Övrigt vetenskapligt)
  • 18.
    Lindfors, Sara
    et al.
    Karolinska Institutet.
    Eintrei, Christina
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Anestesi- och operationscentrum, Intensivvårdskliniken US.
    Alexanderson, Kristina
    Karolinska Institutet.
    Stress factors affecting academic physicians at a university hospital.2009Ingår i: Work (Reading, Mass.), ISSN 1875-9270, Vol. 34, nr 3, s. 305-13Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Research is limited regarding occupational stress in academic physicians; professionals whose work situation includes the three areas of clinical practice, research, and teaching. The aim of this study was to gain knowledge of factors experienced as stressful by academic physicians employed by a university hospital. A questionnaire assessing the frequency and intensity of 36 potentially stressful factors was sent to all 157 academic physicians who were employed at the Linköping University Hospital, Sweden. The response rate was 77%. Both a high frequency and intensity of stress was experienced by 66% of the academic physicians in relation to "time pressure" and by almost 50% in connection with both "find time for research" and having "conflict of interest between different work assignments". Moreover, physicians in the higher age group and those who had attained a higher academic position experienced less stress. The female participants experienced more stress than the males due to gender-related problems and to variables associated with relationships at work. More knowledge is needed to determine the consequences of this finding and to identify coping strategies used for handling such stress.

  • 19.
    Oscarsson, Anna
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Östergötlands Läns Landsting, Anestesi- och operationscentrum, Anestesi- och intensivvårdskliniken VIN.
    Juhas, M.
    Department of Laboratory Medicine, Lund University, Malmö University Hospital, Malmö, Sweden.
    Sjolander, A.
    Sjölander, A., Department of Laboratory Medicine, Lund University, Malmö University Hospital, Malmö, Sweden.
    Eintrei, Christina
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Östergötlands Läns Landsting, Anestesi- och operationscentrum, Intensivvårdskliniken US.
    The effect of propofol on actin, ERK-1/2 and GABAA receptor content in neurones2007Ingår i: Acta Anaesthesiologica Scandinavica, ISSN 0001-5172, E-ISSN 1399-6576, Vol. 51, nr 9, s. 1184-1189Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Aim: Interaction with the ?-aminobutyric acid receptor (GABA AR) complex is recognized as an important component of the mechanism of many anaesthetic agents, including propofol. The aims of this study were to investigate the effect of propofol on GABAAR, to determine whether exposure of neurones to propofol influences the localization of GABA AR within the cell and to look for cytoskeletal changes that may be connected with activation, such as the mitogen-activated protein kinase (MAPK) pathway. Methods: Primary cortical cell cultures from rat, with and without pre-incubation with the GABAAR antagonist bicuculline, were exposed to propofol. The cells were lysed and separated into membrane and cytosolic fractions. Immunoblot analyses of filamentous actin (F-actin), the GABA A ß2-subunit receptor and extracellular signal-regulated kinase-1/2 (ERK-1/2) were performed. Results: Propofol triggers an increase in GABAAR, actin content and ERK-1/2 phosphorylation in the cytosolic fraction. In the membrane fraction, there is a decrease in GABAA ß2-subunit content and an increase in both actin content and ERK-1/2 phosphorylation. The GABAAR antagonist bicuculline blocks the propofol-induced changes in F-actin, ERK and GABA A ß2-subunit content, and ERK-1/2 phosphorylation. Conclusion: We believe that propofol triggers a dose-dependent internalization of the GABAA ß2-subunit. The increase in internal GABAA ß2-subunit content exhibits a close relationship to actin polymerization and to an increase in ERK-1/2 activation. Actin contributes to the internalization sequestering of the GABAA ß2-subunit. © 2007 Acta Anaesthesiol Scand.

  • 20.
    Oscarsson, Anna
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Östergötlands Läns Landsting, Anestesi- och operationscentrum, Anestesi- och intensivvårdskliniken VIN.
    Massoumi, R.
    Department of Laboratory Medicine, Lund University, Malmö University Hospital, Malmö, Sweden.
    Sjolander, A.
    Sjölander, A., Department of Laboratory Medicine, Lund University, Malmö University Hospital, Malmö, Sweden.
    Eintrei, Christina
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Östergötlands Läns Landsting, Anestesi- och operationscentrum, Intensivvårdskliniken US.
    Reorganization of actin in neurons after propofol exposure2001Ingår i: Acta Anaesthesiologica Scandinavica, ISSN 0001-5172, E-ISSN 1399-6576, Vol. 45, nr 10, s. 1215-1220Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: It has previously been shown that propofol in clinically relevant concentrations induces a calcium-dependent conformational change in the cytoskeleton. The aim of this study was to further clarify the effect of propofol on the actin cytoskeleton and to determine if this conformational change is mediated by the interaction between the GABAA-receptor and propofol. Methods: Primary cultured cortical neurons from newborn rats were treated with propofol 3 µg·ml-1 in a time-response titration, with and without preincubation with the GABAA-receptor antagonist, bicuculline. Actin-protein content was detected by Western blot analysis and the cellular content of F-actin measured by a spectrophotometric technique. Results: Propofol triggers a relatively slow statistically significant increase in the intracellular F-actin content, maximum after 20-min incubation (160%±16.3) (mean±SEM) P

  • 21.
    Oscarsson, Anna
    et al.
    Östergötlands Läns Landsting, Sinnescentrum, Intensivvårdskliniken US.
    Oster, Susanne
    Östergötlands Läns Landsting, Sinnescentrum, Intensivvårdskliniken US.
    Fredrikson, Mats
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Yrkes- och miljömedicin. Linköpings universitet, Hälsouniversitetet.
    Lindahl, Tomas
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Klinisk kemi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Diagnostikcentrum, Klinisk kemi.
    Eintrei, Christina
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Sinnescentrum, Intensivvårdskliniken US.
    Platelet function assessed by whole-blood aggregometry in patients undergoing non-cardiac surgery2011Ingår i: EUROPEAN JOURNAL OF ANAESTHESIOLOGY, ISSN 0265-0215, Vol. 28, nr 5, s. 363-369Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background The risk/benefit of continuing low-dose acetylsalicylic acid (aspirin) for secondary prevention in the perioperative period is still debated. The primary aim of this study was to determine the effect of acetylsalicylic acid compared with placebo on platelet function in the perioperative period. Methods This is a subgroup analysis of a randomised, double-blind, placebo-controlled multicentre study. High-risk patients undergoing major non-cardiac surgery were randomised to 75 mg acetylsalicylic acid or placebo 7 days preoperatively, until the third postoperative day. In 36 patients, platelet function in response to arachidonic acid was assessed by whole-blood impedance aggregometry using a multiplate analyser 1 h before surgery, directly after surgery and 48 h postoperatively. Results The platelet function was significantly reduced in patients treated with acetylsalicylic acid compared with placebo in the preoperative period [200 aggregation units (AU) min (interquartile range [IQR] 133-261 AU min(-1)) vs. 860 AU min (IQR 800-1010 AU min), P andlt; 0.001] as well as postoperatively [198 AU min (IQR 138-270 AU min) vs. 605 AU min (IQR 434-836 AU min), Pandlt;0.001]. The platelet response was significantly reduced postoperatively compared with preoperatively in patients receiving placebo [860 AU min (IQR 800-1010 AU min) vs. 605 AU min (IQR 434-861 AU min), P=0.0009]. No significant differences were found between pre- and postoperative platelet function in patients on acetylsalicylic acid [200 AU min (IQR 133-261 AU min) vs. 198 AU min (133-270 AU min), P=0.21]. Conclusion Multiplate whole-blood impedance aggregometry demonstrates acetylsalicylic affect in preoperative as well as postoperative samples derived from patients undergoing non-cardiac surgery.

  • 22.
    Oscarsson Tibblin, Anna
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Anestesi- och operationscentrum, Anestesi- och intensivvårdskliniken VIN.
    Eintrei, Christina
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Anestesi- och operationscentrum, Intensivvårdskliniken US.
    Anskär, S
    Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Linköpings universitet, Hälsouniversitetet.
    Engdahl, Olle
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet.
    Fagerström, Lena
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet.
    Blomqvist, Per
    Anestesikliniken, Ryhov.
    Fredriksson, M
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Yrkes- och miljömedicin. Linköpings universitet, Hälsouniversitetet.
    Swahn, Eva
    Linköpings universitet, Institutionen för medicin och vård, Kardiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärtcentrum, Kardiologiska kliniken.
    Troponin T-values provide long-term prognosis in elderly patients undergoing non-cardiac surgery.2004Ingår i: Acta Anaesthesiologica Scandinavica, ISSN 0001-5172, E-ISSN 1399-6576, Vol. 48, nr 9, s. 1071-9Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: The aim of this study was to evaluate the significance of elevated postoperative Troponin T (TnT) levels in an elderly population undergoing non-cardiac surgery. METHODS: Five hundred and forty-six consecutive patients aged 70 years or older undergoing non-cardiac surgery of >30-min duration were enrolled in this prospective, observational study. A postoperative TnT measurement was obtained on the 5th to 7th postoperative day. Troponin T values greater than 0.02 ng ml(-1) were considered positive. Patients were followed over a 1-year period, and mortality and non-fatal cardiac events (acute myocardial infarction and coronary interventions) were recorded. RESULTS: Troponin T concentrations greater than 0.02 ng ml(-1) were detected in 53 of the study subjects (9.7%). Eleven per cent of the patients with elevated TnT had electrocardiographic or clinical signs of myocardial ischemia. One year after surgery, 17 (32%) of the patients with abnormal TnT concentrations had died. In a multivariate Cox regression analysis adjusting for baseline and perioperative data, a TnT value >0.02 ng ml(-1) was an independent correlate of the mortality adjusted hazard ratio (HR): 14.9 (95% CI 3.7-60.3). Other independent predictors of death were tachycardia (HR, 14.9 95% CI 3.45-64.8), ASA 4 (HR, 8.1 95% CI 1.3-50.0), reoperation (HR, 6.4 95% CI 1.1-36.9), and use of diuretics (HR, 4.2 95% CI 1.3-13.8). CONCLUSION: We conclude that elevated TnT levels in the postoperative period confer a 15-fold increase in mortality during the first year after surgery. Our findings also provide evidence that silent myocardial ischemia is common in an elderly population. Routine perioperative surveillance for TnT might therefore be of use in detecting patients at an increased risk of mortality during the first postoperative year.

  • 23.
    Oscarsson Tibblin, Anna
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Anestesi- och operationscentrum, Anestesi- och intensivvårdskliniken VIN.
    Fredrikson, Mats
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Yrkes- och miljömedicin. Linköpings universitet, Hälsouniversitetet.
    Sorliden, M.
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet.
    Anskär, Stefan
    Linköpings universitet, Institutionen för medicin och hälsa, Kardiologi. Linköpings universitet, Hälsouniversitetet.
    Eintrei, Christina
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Anestesi- och operationscentrum, Intensivvårdskliniken US.
    N-terminal fragment of pro-B-type natriuretic peptide is a predictor of cardiac events in high-risk patients undergoing acute hip fracture surgery2009Ingår i: British Journal of Anaesthesia, ISSN 0007-0912, E-ISSN 1471-6771, ISSN 0007-0912, Vol. 103, nr 2, s. 206-212Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The aim of this investigation was to assess the incidence of elevated N-terminal fragment of pro-B-type natriuretic peptide (NT-proBNP) and its relation to outcome defined as perioperative adverse cardiac events and all-cause mortality in high-risk patients undergoing non-elective surgery for hip fracture. A cohort of patients with hip fractures were extracted from a prospective observational study of high-risk patients (ASA class III or IV) undergoing emergency surgery. NT-proBNP and troponin I were measured before operation. An NT-proBNP greater than= 3984 ng litre(-1) was set as the cut-off level for significance. Perioperative adverse cardiac events and 30 day and 3 month mortality were recorded. Sixty-nine subjects were included. Thirty-four subjects (49%) had an NT-proBNP greater than= 3984 ng litre(-1) before surgery. Thirty-four subjects (49%) had a perioperative adverse cardiac event. Of these, 22 subjects (65%) had NT-proBNP above the diagnostic threshold compared with 12 subjects (34%) who had an NT-proBNP below the diagnostic threshold (P=0.01). Preoperative NT-proBNP greater than= 3984 ng litre(-1) [odds ratio (OR) 3.0; 95% confidence interval (CI) 1.0-8.9] and congestive heart failure (OR 3.0; 95% CI 1.0-9.0) were independent predictors of perioperative adverse cardiac events. A total of eight subjects (12%) died within 30 days after operation. There is a high incidence of elevated NT-proBNP in subjects undergoing non-elective hip fracture surgery. Preoperative NT-proBNP is a valuable predictor of cardiac complications in the perioperative period.

  • 24.
    Oscarsson Tibblin, Anna
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Anestesi- och operationscentrum, Anestesi- och intensivvårdskliniken VIN.
    Fredrikson, Mats
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Yrkes- och miljömedicin. Linköpings universitet, Hälsouniversitetet.
    Sorliden, M
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet.
    Anskär, Stefan
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet.
    Gupta, Anil
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet.
    Swahn, Eva
    Linköpings universitet, Institutionen för medicin och hälsa, Kardiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärtcentrum, Kardiologiska kliniken.
    Eintrei, Christina
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Anestesi- och operationscentrum, Intensivvårdskliniken US.
    Predictors of cardiac events in high-risk patients undergoing emergency surgery2009Ingår i: Acta Anaesthesiologica Scandinavica, ISSN 0001-5172, E-ISSN 1399-6576, Vol. 53, nr 8, s. 986-994Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: The aim of this study was to determine the incidence of myocardial damage and left ventricular myocardial dysfunction and their influence on outcome in high-risk patients undergoing non-elective surgery.

    Methods: In this prospective observational study, 211 patients with American Society of Anesthesiologists classification III or IV undergoing emergent or urgent surgery were included. Troponin I (TnI) was measured pre-operatively, 12 and 48 h post-operatively. Pre-operative N-terminal fragment of B-type natriuretic peptide (NT-proBNP), as a marker for left ventricular systolic dysfunction, was analyzed. The diagnostic thresholds were set to TnI andgt; 0.06 mu g/l and NT-proBNP andgt; 1800 pg/ml, respectively. Post-operative major adverse cardiac events (MACE), 30-day and 3-months mortality were recorded.

    Results: Elevated TnI levels were detected in 33% of the patients post-operatively. A TnI elevation increased the risk of MACE (35% vs. 3% in patients with normal TnI levels, P andlt; 0.001) and 30-day mortality (23% vs. 7%, P=0.003). Increased concentrations of NT-proBNP were seen in 59% of the patients. Elevated NT-proBNP was an independent predictor of myocardial damage post-operatively, odds ratio, 6.2 [95% confidence interval (CI) 2.1-18.0] and resulted in an increased risk of MACE (21% vs. 2.5% in patients with NT-proBNP andlt; 1800 pg/ml, P andlt; 0.001).

    Conclusion: Myocardial damage is common in a high-risk population undergoing unscheduled surgery. These results suggest a close correlation between myocardial damage in the post-operative period and increased concentration of NT-proBNP before surgery. The combinations of TnI and NT-proBNP are reliable markers for monitoring patients at risk in the peri-operative period as well as useful tools in our risk assessment pre-operatively in emergency surgery.

  • 25.
    Oscarsson Tibblin, Anna
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Sinnescentrum, Anestesi- och intensivvårdskliniken VIN.
    Gupta, Anil
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Sinnescentrum, Anestesi- och operationkliniken US.
    Fredrikson, Mats
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Yrkes- och miljömedicin. Linköpings universitet, Hälsouniversitetet.
    Järhult, Johannes
    Linköpings universitet, Institutionen för klinisk och experimentell medicin. Linköpings universitet, Hälsouniversitetet.
    Nyström, Matti
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Sinnescentrum, Anestesi- och intensivvårdskliniken VIN.
    Pettersson, Eva
    Östergötlands Läns Landsting, Anestesi- och operationscentrum, Anestesi- och intensivvårdskliniken VIN.
    Darvish, Bijan
    Department of Anaesthesia & Intensive Care University Hospital, Örebro, Sweden.
    Krook, Helena
    Östergötlands Läns Landsting, Hjärtcentrum, Kardiologiska kliniken.
    Swahn, Eva
    Linköpings universitet, Institutionen för medicin och hälsa, Kardiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärtcentrum, Kardiologiska kliniken.
    Eintrei, Christina
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Sinnescentrum, Intensivvårdskliniken US.
    To continue or discontinue aspirin in the perioperative period: a randomized, controlled clinical trial2010Ingår i: British Journal of Anaesthesia, ISSN 0007-0912, E-ISSN 1471-6771, Vol. 104, nr 3, s. 305-312Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Major adverse cardiac events (MACEs) are a common cause of deathafter non-cardiac surgery. Despite evidence for the benefitof aspirin for secondary prevention, it is often discontinuedin the perioperative period due to the risk of bleeding.

    Methods: We conducted a randomized, double-blind, placebo-controlledtrial in order to compare the effect of low-dose aspirin withthat of placebo on myocardial damage, cardiovascular, and bleedingcomplications in high-risk patients undergoing non-cardiac surgery.Aspirin (75 mg) or placebo was given 7 days before surgery andcontinued until the third postoperative day. Patients were followedup for 30 days after surgery.

    Results: A total of 220 patients were enrolled, 109 patients receivedaspirin and 111 received placebo. Four patients (3.7%) in theaspirin group and 10 patients (9.0%) in the placebo group hadelevated troponin T levels in the postoperative period (P=0.10).Twelve patients (5.4%) had an MACE during the first 30 postoperativedays. Two of these patients (1.8%) were in the aspirin groupand 10 patients (9.0%) were in the placebo group (P=0.02). Treatmentwith aspirin resulted in a 7.2% absolute risk reduction [95%confidence interval (CI), 1.3–13%] for postoperative MACE.The relative risk reduction was 80% (95% CI, 9.2–95%).Numbers needed to treat were 14 (95% CI, 7.6–78). No significantdifferences in bleeding complications were seen between thetwo groups.

    Conclusions: In high-risk patients undergoing non-cardiac surgery, perioperativeaspirin reduced the risk of MACE without increasing bleedingcomplications. However, the study was not powered to evaluatebleeding complications.

     

  • 26.
    Sjöberg, Folke
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Östergötlands Läns Landsting, MKC - Medicin och kirurgicentrum, Anestesi.
    Gustafsson, U
    Eintrei, Christina
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Östergötlands Läns Landsting, MKC - Medicin och kirurgicentrum, Anestesi.
    Specific blood flow reducing effects of hyperoxaemia on high flow capillaries in the pig brain.1999Ingår i: Acta Physiologica Scandinavica, ISSN 0001-6772, E-ISSN 1365-201X, Vol. 165, s. 33-38Artikel i tidskrift (Refereegranskat)
  • 27.
    Suleman Khan, Muhammad
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning. Linköpings universitet, Hälsouniversitetet.
    Zetterlund, Eva-Lena
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning. Linköpings universitet, Hälsouniversitetet.
    Green, Henrik
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning. Linköpings universitet, Hälsouniversitetet. KTH Royal Institute Technology, Sweden.
    Oscarsson, Anna
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning. Linköpings universitet, Hälsouniversitetet.
    Zackrisson, Anna-Lena
    National Board Forens Med, Department Forens Genet and Forens Toxicol, Linkoping, Sweden.
    Svanborg, Eva
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neurovetenskap. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Sinnescentrum, Neurofysiologiska kliniken US.
    Lindholm, Maj-Lis
    Kalmar Hospital, Sweden.
    Persson, Harald
    Kalmar Hospital, Sweden.
    Eintrei, Christina
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Sinnescentrum, Anestesi- och intensivvårdskliniken US.
    Pharmacogenetics, Plasma Concentrations, Clinical Signs and EEG During Propofol Treatment2014Ingår i: Basic & Clinical Pharmacology & Toxicology, ISSN 1742-7835, E-ISSN 1742-7843, Vol. 115, nr 6, s. 565-570Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    A variety of techniques have been developed to monitor the depth of anaesthesia. Propofols pharmacokinetics and response vary greatly, which might be explained by genetic polymorphisms. We investigated the impact of genetic variations on dosage, anaesthetic depth and recovery after total intravenous anaesthesia with propofol. A total of 101 patients were enrolled in the study. The plasma concentration of propofol during anaesthesia was measured using high-performance liquid chromatography. EEG was monitored during the surgical procedure as a measure of anaesthetic depth. Pyrosequencing was used to determine genetic polymorphisms in CYP2B6, CYP2C9, the UGTIA9-promotor and the GABRE gene. The correlation between genotype and to plasma concentration at the time of loss of consciousness (LOC), the total induction dose, the time to anaesthesia, eye opening and clearance were investigated. EEG monitoring showed that the majority of the patients had not reached a sufficient level of anaesthetic depth (subdelta) at the time of loss of consciousness despite a high induction dose of propofol. Patients with UGT1A9-331C/T had a higher propofol clearance than those without (p=0.03) and required a higher induction dose (p=0.03). The patients with UGT1A9-1818T/C required a longer time to LOC (p=0.03). The patients with CYP2C9*2 had a higher concentration of propofol at the time of LOC (p=0.02). The polymorphisms in the metabolizing enzymes and the receptor could not explain the large variation seen in the pharmacokinetics of propofol and the clinical response seen. At LOC, the patients showed a large difference in EEG pattern.

  • 28.
    Turina, Dean
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Anestesiologi.
    Björnström, Karin
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Östergötlands Läns Landsting, Anestesi- och operationscentrum, Intensivvårdskliniken US.
    Eintrei, Christina
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Östergötlands Läns Landsting, Anestesi- och operationscentrum, Intensivvårdskliniken US.
    Orexin A: A propofol antagonist?2005Ingår i: SSAI Congress,2005, 2005Konferensbidrag (Övrigt vetenskapligt)
  • 29.
    Turina, Dean
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Anestesiologi.
    Björnström, Karin
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Östergötlands Läns Landsting, Anestesi- och operationscentrum, Intensivvårdskliniken US.
    Eintrei, Christina
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Östergötlands Läns Landsting, Anestesi- och operationscentrum, Intensivvårdskliniken US.
    Orexin A - An antidot till propofol?2005Ingår i: SFAI-möte,2005, 2005Konferensbidrag (Övrigt vetenskapligt)
  • 30.
    Turina, Dean
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Anestesiologi.
    Björnström, Karin
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Östergötlands Läns Landsting, Anestesi- och operationscentrum, Intensivvårdskliniken US.
    Eintrei, Christina
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Anestesiologi. Östergötlands Läns Landsting, Anestesi- och operationscentrum, Intensivvårdskliniken US.
    Propofol reglerar ansamling av perinukleära GABAa receptorer i korikala råttneuron2006Ingår i: SFAI-möte,2006, 2006Konferensbidrag (Övrigt vetenskapligt)
  • 31.
    Turina, Dean
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Sinnescentrum, Anestesi- och operationkliniken US.
    Björnström-Karlsson, Karin
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Sinnescentrum, Anestesi- och operationkliniken US.
    Sundqvist, Tommy
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Medicinsk mikrobiologi. Linköpings universitet, Hälsouniversitetet.
    Eintrei, Christina
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Sinnescentrum, Intensivvårdskliniken US.
    Propofol alters vesicular transport in rat cortical neuronalcultures2011Ingår i: Journal of Physiology and Pharmacology, ISSN 0867-5910, E-ISSN 1899-1505, Vol. 62, nr 1, s. 119-124Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Neuronal intracellular transport is performed by motor proteins, which deliver vesicles, organelles and proteins along cytoskeletal tracks inside the neuron. We have previously shown that the anesthetic propofol causes dose- and time-dependent, reversible retraction of neuronal neurites. We hypothesize that propofol alters the vesicular transport of cortical neurons due to this neurite retraction. Primary cultures of co-cultivated rat cortical neurons and glial cells were exposed to either 2 mu M propofol, control medium or the lipid vehicle, in time-response experiments. Reversibility was tested by washing propofol off the cells. The role of the GABA(A) receptor (GABA(A)R) was assessed with the GABA(A)R antagonist gabazine. Vesicles were tracked using differential interference contrast video microscopy. Propofol caused a retrograde movement in 83.4 +/- 5.2% (mean +/- S.E.M.) of vesicles, which accelerated over the observed time course (0.025 +/- 0.012 mu m.s(-1)). In control medium, vesicles moved predominantly anterograde (84.6 +/- 11.1%) with lower velocity (0.011 +/- 0.004 mu m.s(-1)). Cells exposed to the lipid vehicle showed the same dynamic characteristics as cells in control medium. The propofol-induced effect on vesicle transport was reversible and blocked by the GABA(A)R antagonist gabazine in low concentration. Our results show that propofol causes a reversible, accelerating vesicle movement toward the neuronal cell body that is mediated via synaptic GABA(A)R. We have previously reported that propofol initiates neurite retraction, and we propose that propofol causes vesicle movement by retrograde flow of cytoplasm from the narrowed neurite.

  • 32.
    Turina, Dean
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet.
    Karin, Björnström Karlsson
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet.
    Sundqvist, Tommy
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Medicinsk mikrobiologi. Linköpings universitet, Hälsouniversitetet.
    Eintrei, Christina
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Sinnescentrum, Intensivvårdskliniken US.
    Orexin A inhibits propofol-induced neurite retraction by a PLD-dependent mechanism in neuronsManuskript (preprint) (Övrigt vetenskapligt)
    Abstract [en]

    Background: Propofol retracts neurites and reverses the transport of vesicles in rat cortical neurons in a γ-aminobutyric acid type A (GABAA) receptor dependent manner. Orexin A (OA) is an endogenous peptide regulating wakefulness, and is known to interact with anaesthetics. We aim to investigate whether OA inhibits propofol-induced neurite retraction and elucidate the intracellular signalling involved.

    Methods: In primary cortical cell cultures from newborn rat brains, live cell light microscopy was used to measure neurite retraction after propofol (2 μM) with or without OA (10 nM) application after preincubation with the Rhokinase inhibitor (HA-1077), phospholipase D (PLD) inhibitor [5-fluoro-2- indolyl des-chlorohalopemide (FIPI)], protein kinase C (PKC) inhibitor (staurosporine) or PKC activator phorbol 12-myristate 13-acetate (PMA).

    Results: The neurite retraction induced by propofol is blocked by HA-1077 and PMA. OA blocks neurite retraction induced by propofol, and this inhibitory effect could be prevented by FIPI, as well as staurosporine.

    Conclusions: Rho-kinase is essential for propofol-induced neurite retraction in cortical neuronal cells. Activation of PKC plays an inhibitive role during neurite retraction caused by propofol. OA blocks propofol-induced neurite retraction by a PLD/PKC-mediated pathway.

  • 33.
    Turina, Dean
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Sinnescentrum, Anestesi- och operationkliniken US.
    Loitto, Vesa
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Medicinsk mikrobiologi. Linköpings universitet, Hälsouniversitetet.
    Björnström, Karin
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Sinnescentrum, Anestesi- och operationkliniken US.
    Sundqvist, Tommy
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Medicinsk mikrobiologi. Linköpings universitet, Hälsouniversitetet.
    Eintrei, Christina
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Sinnescentrum, Anestesi- och operationkliniken US.
    Propofol causes neurite retraction in neurons2008Konferensbidrag (Refereegranskat)
  • 34.
    Turina, Dean
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Sinnescentrum, Anestesi- och operationkliniken US.
    Loitto, Vesa
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Medicinsk mikrobiologi. Linköpings universitet, Hälsouniversitetet.
    Björnström, Karin
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Sinnescentrum, Anestesi- och operationkliniken US.
    Sundqvist, Tommy
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Medicinsk mikrobiologi. Linköpings universitet, Hälsouniversitetet.
    Eintrei, Christina
    Linköpings universitet, Institutionen för medicin och hälsa, Anestesiologi med intensivvård. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Sinnescentrum, Anestesi- och operationkliniken US.
    Propofol causes neurite retraction in neurons2008Ingår i: British Journal of Anaesthesia, ISSN 0007-0912, E-ISSN 1471-6771, Vol. 101, nr 3, s. 374-379Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background The mechanism by which anaesthetic agents produce general anaesthesia is not yet fully understood. Retraction of neurites is an important function of individual neurones and neural plexuses during normal and pathological conditions, and it has been shown that such a retraction pathway exists in developing and mature neurones. We hypothesized that propofol decreases neuronal activity by causing retraction of neuronal neurites.

    Methods Primary cultures of rat cortical neurones were exposed in concentration– and time–response experiments to 0.02, 0.2, 2, and 20 µM propofol or lipid vehicle. Neurones were pretreated with the GABAA receptor (GABAAR) antagonist, bicuculline, the myosin II ATPase activity inhibitor, blebbistatin, and the F-actin stabilizing agent, phalloidin, followed by administration of propofol (20 µM). Changes in neurite retraction were evaluated using time-lapse light microscopy.

    Results Propofol caused a concentration- and time-dependent reversible retraction of cultured cortical neurone neurites. Bicuculline, blebbistatin, and phalloidin completely inhibited propofol-induced neurite retraction. Images of retracted neurites were characterized by a retraction bulb and a thin trailing membrane remnant.

    Conclusions Cultured cortical rat neurones retract their neurites after exposure to propofol in a concentration- and time-dependent manner. This retraction is GABAAR mediated, reversible, and dependent on actin and myosin II. Furthermore, the concentrations and times to full retraction and recovery correspond to those observed during propofol anaesthesia.

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