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OALib Journal期刊
ISSN: 2333-9721
费用：99美元
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热休克反应对高温诱导循环衰竭的防护作用及其机制
, PP. 300-302
Keywords: 热休克反应,热休克蛋白,高温,循环衰竭,丙二醛,一氧化氮
Abstract:
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20h后予以高温热暴露处理,其间监测记录血压、心电。热暴露至73min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73min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73min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。
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