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• W3032646765 abstract "ObjectiveTo evalute the role of phosphatidylinositol 3-kinase(PI3K)/serine-threonine kinase(Akt)/endothelial nitric oxide synthase(eNOS)signaling pathway in sevoflurane postconditioning-induced attenuation of brain injury in a rat model of hemorrhagic shock and resuscitation(HSR).MethodsSeventy-two pathogen-free healthy adult male Sprague-Dawleg rats, weighing 300-350 g, were divided into 4 groups(n=18 each)using a random number table: sham operation group(group S), group HSR, sevoflurane postconditioning group(group SP)and sevoflurane postconditioning plus PI3K/Akt signaling pathway specific inhibitor wortmannin group(group SP+ WT). Hemorrhagic shock was induced by withdrawing blood(40% of the total blood volume)from the right common carotid artery over an interval of 30 min, and 1 h later the animals were resuscitated with infusion of the shed blood via the left jugular vein over 30 min.In group SP+ WT, wortmannin 0.6 mg/kg was administrated via the jugular vein at 30 min before establishment of the model.In SP and SP+ WT groups, 2.4% sevoflurane was inhaled for 30 min starting from the onset of infusion of the shed blood.At 10 min before withdrawing blood(T0), immediately after the end of withdrawing blood(T1), at 30 min and 1 h after the end of withdrawing blood(T2, 3)and immediately after infusion of the shed blood(T4), blood samples from the common carotid artery were collected for blood gas analysis, the blood lactate concentration was recorded, and mean arterial pressure was simultaneously recorded.At 24 h after infusion of the shed blood, 6 rats were randomly selected from each group and sacrificed, and their brains were immediately removed for determination of cerebral infarct volume(by TTC staining), expression of hippocampal caspase-3(by immuno-histochemistry), and expression of Akt, phosphorylated Akt(p-Akt)and eNOS(by Western blot). The ratio of p-Akt/Akt was calculated.ResultsCompared with group S, the mean arterial pressure was significantly decreased and the blood lactate concentration was increased at T1-3, the cerebral infarct volume was increased, and the expression of caspase-3 was up-regulated in the other three groups, and the ratio of p-Akt/Akt was significantly increased, and eNOS expression was up-regulated in group SP(P<0.05). Compared with group HSR, the cerebral infarct volume was significantly decreased, the expression of caspase-3 was down-regulated, the ratio of p-Akt/Akt was increased, and eNOS expression was up-regulated in group SP(P<0.05). Compared with group SP, the cerebral infarct volume was significantly increased, the expression of caspase-3 was up-regulated, the ratio of p-Akt/Akt was decreased, and eNOS expression was down-regulated in group SP+ WT(P<0.05).ConclusionPI3K/Akt/eNOS signaling pathway activation mediates sevoflurane postconditioning-induced attenuation of brain injury in a rat model of HSR.Key words: 1-Phosphatidylinositol 3-kinase; Protein-serine-threonine kinases; Nitric oxide synthase; Anesthetics, inhalation; Ischemic postconditioning; Shock, hemorrhagic; Resuscitation; Brain injuries" @default.
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• W3032646765 date "2018-01-20" @default.
• W3032646765 modified "2023-09-24" @default.
• W3032646765 title "Role of PI3K/Akt/eNOS signaling pathway in sevoflurane postconditioning-induced attenuation of brain injury in a rat model of hemorrhagic shock and resuscitation" @default.
• W3032646765 doi "https://doi.org/10.3760/cma.j.issn.0254-1416.2018.01.018" @default.
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