热休克反应对高温诱导循环衰竭的防护作用及其机制

摘要/Abstract

摘要： 目的探讨热休克反应(HSR)对高温诱导的循环衰竭的保护作用及机制。方法 24只SD大鼠随机分为热休克组、高温对照组和常温对照组3组。热休克组给予热休克预处理,而高温对照组则否。两组常温恢复20 h后予以高温热暴露处理,其间监测记录血压、心电。热暴露至73 min时终止实验,检测心肌丙二醛(MDA)、一氧化氮(NO)含量;运用Chart软件,获取平均动脉压(MAP)、收缩压(SP)、舒张压(DP)、心率(HR)等数据。常温对照组不予任何处理,以获得上述数据的正常值。结果 (1)热暴露73 min时,热休克组与高温对照组动物的MAP、SP、DP值明显低于常温对照组(P<0.01),HR值高于常温对照组(P<0.01)。热休克组与高温对照组相比热休克组表现出更高的MAP、SP、DP(P<0.01)、HR值(P<0.05)。(2) 热暴露73 min时,高温对照组心肌MDA、NO含量显著高于常温对照组(P<0.01)。而此时热休克组心肌MDA含量明显低于高温对照组(P<0.05),并与常温对照组无显著差异。热休克组心肌NO含量亦较高温对照组明显为低(P<0.01)。结论 HSR可减轻高温诱导的循环衰竭,此作用与HSR抑制热暴露大鼠心肌MDA、NO的生成有关。

Abstract: Objective To investigate the preventive effects of heat-shock response (HSR) against circulatory collapse induced by hyperthermia and understand its mechanism. Methods Twenty-four SD rats were randomized equally into heat-shock group (HS group), high temperature control group (HC group) and normal temperature control group (NC group). The rats in HS group, but not HC group, were subjected to heat shock pretreatment. After a recovery period for 20 h at room temperature, the rats in HS and HC groups were exposed to high temperature environment, and their blood pressures and electrocardiograms were measured continuously. Heat exposure was terminated at 73 min and the contents of myocardial malondialdehyd (MDA) and NO were measured. Using Chart software, the data of the mean arterial pressure (MAP), systolic pressure (SP), diastolic pressure (DP), heart rate (HR) were acquired. The rats in NC group did not receive any treatment to obtain the measurements in normal condition. Results Compared with NC group, the MAP, SP and DP were significantly lowered (P<0.01) in HS and HC group and HR accelerated (P<0.01) after a 73-min heat exposure, and HS group had significantly higher measurements of the above indices than HC group did. In comparison with NC group, the contents of MDA and NO in the myocardium in HC group were significantly elevated after the exposure (P<0.01). The MDA content in HS group, which was comparable with that of NC group, was significantly lower than that of HC group (P<0.05), and compared with HC group, HS also had lower NO content (P<0.01). Conclusion HSR may relieve circulatory collapse induced by hyperthermia, which involves the inhibitory effect of HSR on the production of MDA and NO in the myocardium.

中图分类号:

王斌, 罗炳德, 邹飞, 万为人, 郭进强. 热休克反应对高温诱导循环衰竭的防护作用及其机制[J]. 南方医科大学学报, 2004, 24(03): 300-302.

WANG Bin, LUO Bing-de, ZOU Fei, WANG Wei-ren, GUO Jin-qiang. Preventive effects of heat-shock response against circulatory collapse induced by hyperthermia[J]. Journal of Southern Medical University, 2004, 24(03): 300-302.

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