纳洛酮对减轻全脑缺血再灌注后神经元损伤作用的实验研究

目的　探讨纳洛酮对全脑缺血再灌注损伤的防治作用及其机理。方法　96只大鼠随机分为对照组、损伤组和纳洛酮治疗组。采用四血管阻断模型，动态测定脑组织及血浆β-内啡肽(β-EP)、脑组织总钙和脑组织超氧化物歧化酶(SOD)活性、丙二醛(MDA)浓度、脑组织水含量及海马CA1区神经元记数的变化。结果　随再灌注时间的延长，脑组织β-EP水平显著增高，而血浆的变化滞后于脑组织的变化，脑组织总钙水平、MDA浓度、脑组织水含量显著增高，脑组织SOD活性及海马CA1区神经元记数显著降低(P＜0.05和P＜0.01)。使用纳洛酮后上述各指标的异常变化明显减轻，与损伤组比有显著性差异(P＜0.05和P＜0.01)。结论　纳洛酮可减轻全脑缺血再灌注损伤，其机制与拮抗β-EP活性、降低脑组织总钙和氧自由基水平有关。

Experimental study on Naloxone in treating complete brain ischemia-reperfusion injury

Objective To explore the protective of Naloxone hydrochloride onbrain and its mechanism during complete brain ischemia-reperfusion injury.Methods Ninety-six rats were randomized into the control group,ischemia/reperfusion injury group(IR) and Naloxone-treated group.The dynamic changes of β-EP in brain tissue and in plasma were observed.The total calcium、superoxide dismutase(SOD)、malondialdehyde(MDA)、water content of the brain tissue and the count of neurons in hippocampal CA1 were also measured.Results β-EP level in brain tissues increased remarkably(P＜0.05 and P＜0.01),the alterations of β-EP in plasma lagged it in brain tissues.The total calcium level、MDA content and water content of the brain tissues increased remarkably,the SOD activity and the count of neurons in hippocampal CA1 decreased significantly(P＜0.05 and P＜0.01),in Naloxone-treating group,the abnormal changes of indexes as above were ameliorated markedly,and there was significant difference between IR group and Naloxone group(P＜0.05 and P＜0.01).Conclusion Naloxone could attenuate complete brain ischemia-reperfusion injury,the mechanism was related to its contradicting β-EP activity and reducing the total calcium and oxygen free radicals.