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目的观察不同高温环境中热应激大鼠心肌损伤状况,探索血液淋巴细胞中HSP70水平与心肌损伤的相关性规律及其意义。方法 50只雄性Wistar大鼠随机分为常温(22～25℃)组,36、37、38、39℃热应激组。以人工高温舱对大鼠进行热暴露。采用电子肛温计检测大鼠肛温,采用八导生理记录仪观测大鼠心电图的变化,采用酶学试剂盒检测大鼠血清乳酸脱氢酶(LDH)和肌酸激酶同工酶(CK-MB)活力,采用Western Blot方法对大鼠外周血淋巴细胞热休克蛋白70(HSP70)含量进行半定量分析。结果与常温组比较,36~39℃组体温均升高(均P<0.05);37~39℃组Q-T间期延长和R波振幅下降(均P<0.05);38~39℃组血清中LDH和CK-MB活力升高(均P<0.05)。淋巴细胞中HSP70表达水平随环境温度的变化呈现不同的变化规律,热环境温度≤37℃时,HSP70表达随气温升高而显著增加(均P<0.05),热环境温度≥38℃后,HSP70表达随气温升高而下降,但仍显著高于常温组(均P<0.05)。结论热应激可导致大鼠心肌损伤和外周血淋巴细胞HSP70表达水平发生规律性变化,提示HSP70可能是热应激致心肌损伤的一种生物标志分子,在高温所致心肌损伤发生中具有重要作用。
Objective To observe the myocardial damage induced by heat stress in different high temperature environments and to explore the correlation between the HSP70 level and myocardial injury in blood lymphocytes and its significance. Methods Fifty male Wistar rats were randomly divided into normal temperature (22 ~ 25 ℃) group, 36, 37, 38, 39 ℃ heat stress group. Rats were exposed to heat in an artificial hot chamber. The rectal temperature was detected by electronic rectal thermometer. The changes of electrocardiogram (ECG) in rats were observed by using eight-lead electrophoresis recorder. Serum lactate dehydrogenase (LDH) and creatine kinase (CK- MB), and Western Blot method was used to semi-quantitatively analyze the content of heat shock protein 70 (HSP70) in peripheral blood lymphocytes of rats. Results Compared with the normal temperature group, the body temperature of 36 ~ 39 ℃ group increased (all P <0.05); the QT interval prolonged and the amplitude of R wave decreased in 37 ~ 39 ℃ group (all P <0.05) LDH and CK-MB increased (all P <0.05). The expression of HSP70 in lymphocytes changed differently with the change of ambient temperature. When the ambient temperature was less than 37 ℃, the expression of HSP70 increased significantly with the increase of temperature (all P <0.05) Expression decreased with increasing temperature, but still significantly higher than normal temperature group (all P <0.05). Conclusion Heat stress can cause myocardial injury in rats and regular expression of HSP70 in peripheral blood lymphocytes, suggesting that HSP70 may be a biomarker molecule induced by heat stress and play an important role in myocardial injury induced by hyperthermia effect.