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其机制。方法 本研究分为 2个实验 :(1)HSR的保护作用。大鼠分为 2组 :热休克组、对照组。热休克组予热休克预处理 ,对照组则否。两组常温恢复 2 0h后予以热暴露至死亡 ,监测记录血压、心电。运用Chart软件获取平均动脉压 (MAP)、生存时间等数据。 (2 )作用的机制。大鼠分为 3组 :热休克组、对照组和常温对照组。常温对照组不予任何处理。前两组处理同实验一 ,但在热暴露至 73min时终止实验 ,记录收缩压 (Ps)、舒张压 (Pd)等数据 ,并检测心肌一氧化氮 (NO)、热休克蛋白 (HSP70 )含量。结果 热休克组生存时间 [(10 2 .3± 11.4 )min]明显长于对照组 [(87.9± 7.7)min],且休克出现晚 ,差异有显著性 (P <0 .0 1)。热暴露早期热休克组与对照组MAP差异无显著性 (P >0 .0 5 ) ,6 0min后 ,前者高于后者。热暴露至 73min时 ,热休克组MAP、Ps、Pd、HR均较对照组明显升高 ,差异有显著性 (P <0 .0 5、P <0 .0 1) ,心肌HSP70、NO含量则较对照组明显降低 ,差异亦有显著性 (P <0 .0 1)。结论 HSR可能通过诱导心肌HSP70的高表达 ,抑制热暴露大鼠心肌NO过量生成 ,从而减轻高温诱导的循环衰竭。
Objective To investigate the protective effects and mechanism of heat shock response(HSR) on circulatory collapse induced by hyperthermia. Methods Two experiments were carried out:(1)Protective effects of HSR.Rats were divided into 2 groups:heat shock(HS) group,sham control(SC) group.After HS group was pretreated with heat shock and recovered for 20 h at room temperature,both groups were exposed to heat till death,and blood pressure,electrocardiogram were measured continuously during exposure.Mean arterial pressure(MAP),survival time etc were acquired through Chart software.(2)Mechanism of effects.Rats were divided into 3 groups: HS group,SC group and normal control(NC) group.The treatment in HS and SC groups was identical with that in the first experiment,but it would be terminated at 73 min after heat exposure.Systolic pressure(Ps),diastolic pressure(Pd) etc were recorded and content of NO and HSP70 in myocardium were measured. Results (1)The survival time in HS group[(102.3±11.4)min] was longer than that in SC group[(87.9±7.7)min] and shock revealed later(P<0.01);(2)During early heat exposure MAP in HS group was not different from that in SC group,but after 60 min MAP in HS group were higher than that in SC group;(3)MAP,Ps,Pd,HR and HSP70 in HS group were significantly higher but content of NO was lower than those in SC group(P<0.01,P<0.05). Conclusion HSR may induce upregulation of HSP70 and inhibit excessive production of NO in myocardium,thus result in relief of circulatory collapse induced by hyperthermia.
出处
《中华劳动卫生职业病杂志》
CAS
CSCD
北大核心
2004年第2期115-118,共4页
Chinese Journal of Industrial Hygiene and Occupational Diseases
基金
"十五"军队指令性课题 ( 0 1L0 5 1)