Objective Isoflurane has an acute preconditioning effectiveness against ischemia in kidney, but this beneficial effectiveness can only last for 2-3 hours. To investigate whether isoflurane produces delayed preconditioningagainst renal ischemia/reperfusion (I/R) injury, and whether this process is mediated by hypoxia inducible factor 1α(HIF- 1α). Methods A total of 52 male C57BL/6 mice were randomly assigned to 4 groups (n=13 in each group): the controlgroup (group A), PBS/isoflurane treated group (group B), scrambled small interference RNA (siRNA)/isoflurane treated group (group C), and HIF-1α siRNA/isoflurane treated group (group D). In groups C and D, 1 mL RNase-free PBS containing 50 μg scrambled siRNA or HIF-1α siRNA was administered via tail vein 24 hours before gas exposure, respectively. Equivalent RNasefree PBS was given in groups A and B. Then the mice in groups B, C, and D were exposed to 1.5% isoflurne and 25%O2 for 2 hours; while the mice in group A received 25%O2 for 2 hours. After 24 hours, 5 mice in each group were sacrificed to assesse the expressions of HIF-1α and erythropoietin (EPO) in renal cortex by Western blot. Renal I/R injury was induced with bilateral renal pedicle occlusion for 25 minutes followed by 24 hours reperfusion on the other 8 mice. At the end of reperfusion, the serum creatinine (SCr), the blood urea nitrogen (BUN), and the histological grading were measured. Results The expressions of HIF-1α and EPO in groups B and C were significantly higher than those in group A (P lt; 0.01). The concentrations of SCr and BUN in groups B and C were significantly lower than those in group A, as well as the scores of tubules (P lt; 0.01), and the injury of kidney was amel iorated noticeably in groups B and C. The expressions of HIF-1α and the concentrations of SCr and BUN in group D were significantly lower than those in group A (P lt; 0.01). Compared with groups B and C, the expression of HIF- 1α and EPO in group D decreased markedly (P lt; 0.01), the concentrations of SCr and BUN were increased obviously, as well asthe scores of tubules (P lt; 0.01), and the renal injury was aggratived significantly. Conclusion Isoflurane produces delayed preconditioning against renal I/R injury, and this beneficial effectiveness may be mediated by HIF-1α.
目的 探讨异氟醚通过抑制细胞间黏附分子（ICAM-1）表达参与减轻肝脏缺血-再灌注（IR）损伤的可能调节机制。 方法 32只雌性SD大鼠分为4组。A组大鼠行腹腔注射1%戊巴比妥钠40 mg/kg麻醉，进行手术但不阻断入肝血流；B组1%戊巴比妥钠麻醉后行部分肝脏IR；C组大鼠仅接受1.0 MAC异氟醚吸入麻醉，不阻断血流；D组采用1.0 MAC异氟醚麻醉，建立肝脏IR模型。肝脏缺血60 min，再灌注3 h后取肝组织和血液标本，检测血清丙氨酸转氨酶（ALT）和天冬门氨酸转氨酶（AST）、肝组织ICAM-1和肝组织还原型谷胱甘肽（GSH）、脂质过氧化物丙二醛（MDA）和超氧化物歧化酶（SOD）含量。 结果 与戊巴比妥钠麻醉比较，采用异氟醚处理后明显降低血清ALT和AST的水平，再灌注肝组织内GSH、SOD含量明显高于而MDA含量降低，同时抑制肝组织ICAM-1的表达。 结论 异氟醚麻醉能够有效减轻肝脏IR损伤，抑制氧自由基的生成和释放，具体机制可能与抑制ICAM-1表达致使细胞内GSH含量增加密切相关。
目的 探讨异氟醚吸入麻醉对（SD）老年大鼠学习和记忆的影响。 方法 36只SD健康雄性大鼠随机分为异氟醚麻醉组和对照组，每组各18只。麻醉组给予2%异氟醚和40%氧气诱导及维持麻醉3 h，对照组单纯吸入含40%氧气的空氧混合气体3 h。麻醉组或对照组干预结束24 h后开始为期1周的盲法测试学习记忆能力。 结果 麻醉组大鼠与对照组大鼠相比，Y-迷宫测试成绩错误反应次数差异无统计学意义（P＞0.05）；除第7天麻醉组大鼠起步电压高于对照组（P＜0.05）外，其余时间两组大鼠起步电压差异均无统计学意义（P＞0.05）；除第3天麻醉组大鼠跑步电压高于对照组（P＜0.05）外，其余时间两组大鼠跑步电压差异均无统计学意义（P＞0.05）。 结论 2%单纯异氟醚吸入麻醉不改变老年大鼠麻醉后学习和记忆能力。
ObjectiveTo investigate whether emulsified isoflurane applied after an ischemic episode induces postconditioning in an ischemia model of myocardial injury and its underlying mechanism. MethodsBetween March and October 2012, using a model of in situ myocardial ischemia and reperfusion injury in rats, cardioprotective effects of emulsified isoflurane were examined by determining infarct size, myocardial damage markers and the concentration of tumor necrosis factor (TNF)-α. ResultsEmulsified isoflurane postconditioning limited infarct size compared with control groups. It increased serum concentrations of superoxide dismutase while decreased malonaldehyde. TNF-α positive cells were also significantly reduced in emulsified isoflurane group compared with control group. Infusion of intralipid had no effect on infarct size or other variables. ConclusionIntravenous administration of emulsified isoflurane after reperfusion protects hearts against reperfusion injury, which may be mediated by the inhibition of cardiac damage markers and the concentration of TNF-α.