药物预处理对沙土鼠缺血再灌注损伤脑组织的保护作用

The Protective Effect of Pretreatment with Two Medicines on Cerebral Tissue of Mongolian Gerbils Injured by Cerebral Ischemia-reperfusion

目的:比较利多卡因、异丙酚预处理对沙土鼠脑缺血再灌注损伤的脑保护作用。方法:沙土鼠34只,随机分为正常对照组、缺血损伤组、利多卡因预处理组、异丙酚预处理组,预处理组脑在缺血前24h分别予利多卡因30mg/kg及异丙酚100mg/kg腹腔注射,对照组7只,余每组为9只,观察指标为超氧化物岐化酶(SOD)、谷光甘肽(GSH)的活性及丙二醛(MDA)、内皮素(ET)、降钙素基因相关肽(CGRP)的含量。每组随机取一左大脑皮层的1mm×1mm组织块作电镜检查,观察脑组织超微结构的改变。结果:利多卡因及异丙酚预处理组的SOD,GSH的活性高于缺血损伤组(P<0.01或P<0.05),而MDA,ET的含量低于缺血损伤组(P<0.01或P<0.05),CGRP的含量虽高于缺血损伤组,但两者的差别不具有统计学意义(P>0.05),两组预处理组之间比较差异无显著性;与缺血损伤组比较,两预处理组的脑组织超微结构损伤有不同程度的改善,两预处理组的改变差异无显著性。结论:缺血前24h予利多卡因预处理及异丙酚预处理对沙土鼠的脑缺血再灌注损伤有不同程度的减轻作用,这种作用可能与其增加体内抗氧化物质SOD,GSH的活性及拮抗ET的毒性有关。两种预处理的保护作用无明显差异。

Objective: To study the protective effects of lidocaine and propofol pretreatment to cerebral tissue of gerbils undergone schemia-reperfusion injury. Methods:Thirty-four Mongolian gerbils were randomly divided into four groups:A)Control group with sham operation( n =7);B)ischemia group ( n =9);C)Lidocaine pretreatment group( n =9);D)Propofol pretreatment group( n =9).Lidocaine 30 mg/kg or propofol 100 mg/kg were given to the animals in groups C and D respectively(ip)24 h before ischemia. Ischemia-reperfusion operation:clamping bilatered common carotid arteries for 10 min after the animals were anesthetized with urethane at the dose of 1 g/kg ip,and then unclamped for reperfusion for 50 min.The animals in group A were only exposed with their bilatered common carotid arteries but not clamped.Detection procedures:The animals were decapitated and forebrain cerebral cortex was removed for the determination of superoxid dismutase(SOD)and glutathione(GSH)activities and contents of malondial dehyde(MDA),endothelin(ET)and calcitonin gene-related peptide(CGRP).One sample of left forebrain cerebral cortex (1 mm×1 mm) was removed randomly in each group to observe the ultramicroscopic changes of cerebral tissue with electronic microscope. Results: MDA and ET contents were significantly lower and SOD,GSH activities were higher in groups C and D than those in group B ( P <0.01, P <0.05, P <0.01, and P <0.05, respectively); CGRP contents in groups C and D were higher than those in group B, but the differences were not significant statistically( P >0.05). No significant difference was found between two pretreatment groups. Compared with group B, the ultramicroscopic pathological changes of cerebral tissue structures were lighter to different degrees in groups C and D, and there was no difference between the latter two groups in respect of pathological changes. Conclusions: Lidocaine and propofol pre-treatment 24 h before cerebral ischemia might have effects to some degree to protect cerebral tissue from ischemia-reperfusion caused injury. The protection has relation to the rise of SOD, GSH activities and the decrease of ET. The protection results are not significantly different between the pretreatments of the two medicines.