摘要
目的 :研究热休克预处理对 SD大鼠再灌注性心律失常的影响及其作用机制。 方法 :将 32只 SD大鼠随机分为热休克组 (n=16 )和对照组 (n=16 )。热休克组大鼠给予热休克预处理而对照组则否。采用 L angendorff离体心脏灌注法 ,先稳定灌注 40分 ,再停灌 2 0分 ,然后复灌 6 0分。心电图记录再灌注时心律失常情况。并检测再灌注时心脏流出液肌酸激酶 (CK)的活性。以 Western blot法检测两组心脏组织中 70 KD热休克蛋白(HSP70 )的相对含量。另外还检测心肌组织中的超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶 (GSH- Px)和过氧化氢酶(CAT)等抗氧化酶的活性 ,及脂质过氧化物丙二醛 (MDA)的含量。 结果 :热休克组的再灌注性心律失常发生率明显较对照组为低 ,表现为心室颤动发生率在热休克组为 0 ,而对照组为 6 / 16。室性心动过速发生率热休克组为 3/ 16 ,而对照组为 7/ 16 ,以热休克组为低 (P<0 .0 5 )。再灌注过程中心肌 CK的释放量热休克组 31.4± 6 .8IU/ L 较对照组 42 .3± 8.9IU/ L显著减少 (P<0 .0 0 1)。热休克组心脏组织 HSP70表达量较对照组显著增多 ,信号条带积分吸光值热休克组为 6 .39± 1.98,对照组为 4.6 2± 2 .0 5 (P<0 .0 1)。热休克组抗氧化酶活性较对照组明显增强 ,而脂质过氧化物则降?
Objective:To investigate the effect and mechanism of heat shock response on reperfusion arrhythmias (RAs) in rat. Methods:Thirty two Sprague Dawley rats were randomly divided into 2 groups:the heat shock group (group H) and the control group (group C).Twenty four hours after heat shock preconditioning,the hearts of rats in group H were excised and mounted on a non circulating Langendorff perfusion apparatus and perfused retrogradely with modified K H buffer.After perfused for a stable period of 40 min,global ischemia was induced for 20 min followed by 60 min reperfusion.The rats in group C were treated similarly as that in group H except that they needn't to be preconditioned with heat shock.RAs were recorded and the effluent during reperfusion was collected for measurement of creatine kinase (CK).Finally the hearts were stored in liquid nitrogen for measurement of heat shock protein(HSP) 70 (by Western bloting),the activity of anti oxydase (SOD,GSH Px,CAT) and lipid peroxydative products MDA. Results:Prior heat stress significantly decreased reperfusion arrhythmias.No ventricular fibrillation (VF) was seen in group H,while the incidence of VF in group C was 6/16.The incidence of ventricular tachycardia (VT) in group H was 3/16 while 7/16 in group C( p <0 05).The amount of CK release in the effluent in group H was much less than that in group C(31 4±6 8 IU/L vs.42 3±8 9 IU/L, p <0 001).Myocardial HSP70 content was elevated significantly in group H.Optical density ratios of group H and C were 6.39±1.98 vs.4.62±2.05 ( p <0.01).Additionally,heat stress significantly increased myocardial anti oxydases activity and decreased lipid peroxydative products. Conclusion:Heat shock pretreatment markedly reduces ischemia/reperfusion induced injury of heart and ventricular arrhythmias in rat and this effect is associated with the increase of myocardial HSP70 and activity of anti oxydase activity.
出处
《中国循环杂志》
CSCD
北大核心
2001年第1期21-23,共3页
Chinese Circulation Journal
基金
国家自然科学基金!资助项目 (39570 31 6)