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目的研究异氟醚、七氟醚和地氟醚预处理对脑缺血再灌注损伤大鼠海马CBS／H2S、iNOS／NO和HO-1／CO的影响,探讨吸入麻醉药脑保护作用的机制。方法30只Wistar大鼠随机分为5组(n=6):对照组(C组)、脑缺血再灌注组(I／R组)、异氟醚组(Ⅰ组)、七氟醚组(S组)和地氟醚组(D组)。采用四动脉阻断法建立大鼠全脑缺血再灌注模型。Ⅰ组、S组和D组夹闭两侧颈总动脉前分别吸入氧气+0．65 MAC的异氟醚、七氟醚和地氟醚30 min,C组和I／R组吸入氧气。缺血20 min,再灌注12 h后处死大鼠,取海马,测定大鼠海马组织中H2S、NO、CO、cAMP和cGMF。含量和CBS、iNOS和HO活性以及CBS—mRNA、iNOS—mRNA和HO-1-mRNA的表达水平;电镜下观察海马线粒体的变化。结果与C组相比,I／R组海马组织CO、H2S、NO、cAMP、cGMP含量和HO、CBS、iNOS活性升高,CBS-mRNA、iNOS-mRNA和HO-1-mRNA表达升高,海马神经细胞线粒体变性率升高(P<0．01);与I／R组相比,Ⅰ组、D组和S组CO含量和HO活性升高,H2S、NO、cAMP含量和CBS、iNOS活性降低,CBS—mRNA和iNOS-mRNA表达降低而HO-1-mRNA表达升高,线粒体变性率降低(P<0．05或0．01)。结论异氟醚、七氟醚和地氟醚预处理可通过抑制CBS／H2S、iNOS／NO,激活HO-1／CO,减轻了大鼠脑缺血再灌注损伤。
Objective To investigate the effects of isoflurane, sevoflurane and desflurane pretreatment on CBS / H2S, iNOS / NO and HO-1 / CO in hippocampus of rats with cerebral ischemia-reperfusion injury and to explore the mechanism of inhalation anesthetics on cerebral protection . Methods Thirty Wistar rats were randomly divided into five groups (n = 6): control group (C group), cerebral ischemia reperfusion group (I / R group), isoflurane group (group Ⅰ), sevoflurane group (Group S) and desflurane group (group D). A rat model of global cerebral ischemia-reperfusion was established by four-artery occlusion method. Group Ⅰ, group S and group D inhaled oxygen + 0.65 MAC of isoflurane, sevoflurane and desflurane respectively for 30 min before occlusion of common carotid artery on both sides. Group C and I / R inhaled oxygen. Twenty minutes after ischemia and 12 hours after reperfusion, the rats were sacrificed and the hippocampus was taken for determination of H2S, NO, CO, cAMP and cGMF in the hippocampus of rats. Content, CBS, iNOS and HO activity as well as the expression of CBS-mRNA, iNOS-mRNA and HO-1-mRNA. The changes of mitochondria in hippocampus were observed under electron microscope. Results Compared with group C, the content of CO, H2S, NO, cAMP, cGMP and the activity of HO, CBS and iNOS in hippocampus of I / R group were increased and the expression of CBS-mRNA, iNOS-mRNA and HO- The mitochondrial degeneration rate of hippocampal neurons increased (P <0.01). Compared with I / R group, the content of CO and the activity of HO increased in group Ⅰ, group D and group S, while the content of H2S, NO and cAMP, CBS-mRNA and iNOS-mRNA expression decreased while HO-1-mRNA expression increased and mitochondrial degeneration rate decreased (P <0.05 or 0.01). Conclusion Isoflurane, sevoflurane and desflurane preconditioning can attenuate cerebral ischemia-reperfusion injury in rats by inhibiting CBS / H2S, iNOS / NO and activating HO-1 / CO.