| 1. |
- Bravo, L, et al.
(författare)
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- 2021
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swepub:Mat__t
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| 2. |
- Tabiri, S, et al.
(författare)
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- 2021
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swepub:Mat__t
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| 3. |
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| 4. |
- Björnström, Karin, 1971-, et al.
(författare)
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Characterisation of the signal transduction cascade caused by propofol in rat neurons : From the GABAA receptor to the cytoskeleton
- 2008
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Ingår i: Journal of Physiology and Pharmacology. - 0867-5910 .- 1899-1505. ; 59:3, s. 617-632
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Tidskriftsartikel (refereegranskat)abstract
- 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.
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| 5. |
- Björnström-Karlsson, Karin, et al.
(författare)
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Orexin A Inhibits Propofol-Induced Neurite Retraction by a Phospholipase D/Protein Kinase C-epsilon-Dependent Mechanism in Neurons
- 2014
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Ingår i: PLOS ONE. - : Public Library of Science. - 1932-6203. ; 9:5, s. e0097129-
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Tidskriftsartikel (refereegranskat)abstract
- 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.
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| 6. |
- Protic, Alen, et al.
(författare)
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Effect of preoperative feeding on gastric emptying following spinal anesthesia: a randomized controlled trial
- 2010
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Ingår i: WIENER KLINISCHE WOCHENSCHRIFT. - : Springer Science and Business Media LLC. - 0043-5325 .- 1613-7671. ; 122:1-2, s. 50-53
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Preoperative fasting is associated with various untoward postoperative health problems. Previous studies have stressed the advantages of preoperative feeding with a carbohydrate-rich drink 2 hours before surgery; this protocol does not increase the risk of gastric-content aspiration but reduces the level of anxiety and thirstiness during the perioperative period. Spinal anesthesia with the local anesthetic bupivacaine can decrease gastric emptying in the early postoperative period. However, the effect of spinal anesthesia on the gastric emptying rate following preoperative feeding is unknown. The aim of this study was to determine the impact of preoperative feeding with a clear carbohydrate-rich drink on gastric emptying early after orthopedic surgery under spinal anesthesia. METHODS: A total of 110 patients scheduled for semi-elective orthopedic surgery under spinal anesthesia were included in a randomized controlled trial. Patients were randomly assigned to two groups: group 1 (56 patients) received a standardized 200 ml of clear carbohydrate-enriched drink orally 2 hours before surgery; group 2 (54 patients) acted as a control group with no preoperative feeding. Gastric emptying was evaluated with a paracetamol test at five time points: 15 min, 30 min, 60 min, 90 min and 120 min after administration of paracetamol. RESULTS: No significant differences were observed between the two groups in paracetamol plasma concentrations or area under the curve during the early postoperative period. CONCLUSION: In patients undergoing spinal anesthesia, preoperative feeding 2 hours before surgery had no influence on the gastric emptying rate, indicating that preoperative feeding does not increase the risk of gastric-content aspiration and can be given safely.
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| 7. |
- Turina, Dean, et al.
(författare)
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Mechanisms of general anesthetic action : Focus on the cellular network
- 2011
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Ingår i: TRANSLATIONAL NEUROSCIENCE. - : VERSITA, SOLIPSKA 14A-1, 02-482 WARSAW, POLAND. - 2081-3856 .- 2081-6936. ; 2:2, s. 168-175
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Tidskriftsartikel (refereegranskat)abstract
- The discovery of general anesthetics had a tremendous impact on development of surgery and medicine in general, during the last century. Despite the widespread use of general anesthetics, the mechanisms by which they produce their effects in the central nervous system are still poorly understood. Over the past decade, several new findings have contributed significantly to a better understanding of general anesthetic mechanisms. The current review summarizes recent data on different anesthetic neuronal targets that might be involved in the mechanism of action of general anesthetics, giving special attention to the importance of binding pockets for anesthetics within transmembrane receptors and cellular signaling leading to morphological changes of neuronal cells. Several lines of evidence suggest that disruption in brain network connectivity is important for anaesthesia-induced loss of consciousness and this is discussed in relation to morphological changes.
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| 8. |
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| 9. |
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| 10. |
- Turina, Dean, 1966-, et al.
(författare)
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Orexin A inhibits propofol-induced neurite retraction by a PLD-dependent mechanism in neurons
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- 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.
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