二氮嗪预处理对深低温停循环脑组织超微结构与自由基的影响  

Effects of Preconditioning With Diazocide on Cerebral Ultrastructure and Free Radical Induced by Deep Hypothermic Circulatory Arrest

作　　者：高国栋[1] 龙村[1] 李明[2] 田良鑫[2] 郑军[2] 

机构地区：[1]中国医学科学院阜外心血管病医院体外循环科,北京100037 [2]中国医学科学院阜外心血管病医院外科,北京100037

出　　处：《中国体外循环杂志》2005年第1期31-33,36,共4页Chinese Journal of Extracorporeal Circulation

基　　金："十五"攻关(2002-1506)

摘　　要：目的　观察二氮嗪预处理对深低温停循环(DHCA)兔脑组织超微结构与自由基的影响。方法　健康大耳白兔 24只,随机分为 3组,对照组(安慰剂组n=8):DHCA+安慰剂;实验组 (二氮嗪组n=8 ):DHCA+二氮嗪(二氮嗪 5mg/kg,CPB前 15min静脉注入);拮抗剂组(5-HD组n=8):DHCA+5-HD(20mg/kg,给予二氮嗪前静脉注入) +二氮嗪(5mg/kg,CPB前 15min静脉注入)。每组均经CPB降温至鼻咽温 18℃,停循环 60min,复温,停机,取脑组织。硫代巴比妥酸法和黄嘌呤氧化酶法测定脑组织匀浆MDA含量和SOD活性,透射电镜观察脑组织超微结构的改变。结果　实验组脑组织MDA含量明显低于对照组 (P<0. 01)及拮抗剂组 (P<0. 05);实验组SOD活性明显高于对照组(P<0. 01)及拮抗剂组(P<0. 05);拮抗剂组MDA含量和SOD活性与对照组比无统计学意义(P>0. 05);电镜结果示各组脑细胞超微结构明显损伤,总体印象实验组各种神经元细胞器损伤较对照组与拮抗剂组有所减轻。结论　二氮嗪预处理对DHCA引起的神经元损伤具有早期保护作用。OBJECTIVE To investigate whether preconditioning with diazoxide could ameliorate the cerebral injuries induced by deep hypothermic circulatory arrest (DHCA). METHODS Twenty-four rabbits weighting 2.3-2.8kg were randomly allocated to 3 groups, each group consists of eight rabbits. One group served as control: received DHCA and vehicle. In experiment group animals received DHCA and preconditioning with diazoxide (5mg/kg bolus 15 minutes prior to CPB) . In antagonist group animals received DHCA 、preconditioning with diazoxide (5mg/kg, bolus 15 minutes prior to CPB ) and mitoKATP antagonists, 5-hydroxydecanoic acid (5-HD, 20mg/kg, before diazoxide administration). Each group was placed on cardiopulmonary bypass (CPB) and cooled to 18℃. After 60 minters of DHCA, animals were rewarmed and weaned from CPB. All animals were executed at the end of experience and brain tissue was removed for ultrastrucrure examination and measurement of the content of malondialdehyde (MDA) and superoxide dismutase (SOD) activity in brain tissue.RESULTS In experiment group, the activity of SOD increased significantly and the content of MDA in brain tissue decreased significantly as compared with that in control group and antagonist group(P<0.05) . Distinct cerebral untrastructural injuries were seen in the three groups on transmission microscopy. Overall quality level, the injury in control group and in antagonist group was more severe than that in experiment group. CONCLUSION Preconditioning with diazoxide protects brain from ischemia-reperfusion injury induced by DHCA. This suggests that pharmacologic preconditioning with the mitoKATP channel opener diazoxide may offer effective neuroprotection.

关 键 词：脑组织 二氮嗪 DHCA 对照组 拮抗剂 超微结构 深低温停循环 静脉 CPB 自由基 

分 类 号：R654.1[医药卫生—外科学]