热射病大鼠死亡危险因素及心肌损伤的实验研究

摘要

目的 复制热射病(HS)大鼠模型,探讨HS大鼠死亡危险因素及心肌损伤情况.方法 雄性无特定病原体级SD大鼠48只,随机分为对照组、HS组、维生素E组(HS维生素E处理)、缬沙坦组(HS缬沙坦处理),每组12只;除对照组外,余组给予40℃、(65±1)%湿热打击,达复制模型标准后终止;心肌苏木精-伊红染色法(HE)染色及透射电镜观察病理变化.结果 对照组体重变化率与其余3组比较,差异有统计学意义(<0.05),HS组血清乙酰胆碱(Ach)含量为(9.958±4.283)μg/ml,对照组为(15.734±4.987)μg/ml,两组比较,差异有统计学意义(<0.05);HE染色和透射电镜结果显示,HS大鼠存在心肌损伤,且维生素E组、缬沙坦组大鼠心肌损伤程度较HS组减轻.结论 死亡事件主要发生在发病后24 h内,且低体温和较长打击时间是大鼠死亡的主要危险因素,但相对较高的体重变化率是大鼠存活的保护因素;HS大鼠存在心肌损伤,其潜在机制可能是氧化应激和血管紧张素Ⅱ诱导的心肌细胞凋亡.%Objective To establish the rat model of heat stroke, explore the risk factors of death and myocardium injury in the rat model. Methods Forty-eight male SD rats of SPF grade were randomly divided into group of blank control (C), group of heat stroke (HS), group of heat stroke vitamin E treatment (VitE) and group of heat stroke Valsartan treatment (Valsartan), each group included 12 rats. Except the group C, the rats of other groups were put in a damp and hot environment of 40℃ (temperature) and (65 ± 1) %(humidity) until the standard of the model of heat stroke was reached. The core temperature of the bodies of rats were monitored via the record of rectal temperature. The responses of heat stress in the HS, VitE HS and Valsartan HS groups and the survival time of rats were analyzed and compared by K-M survival analysis. The risk factors of survival were analyzed by univariate and multivariate Cox regression analyses. The lesions of myocardium were observed through HE staining and transmission electron microscopy (TEM). Results The rate of weight change in the group C was significantly lower than that in the groups HS, VitE HS and Valsartan HS ( <0.05). The serum level of acetylcholine (Ach) in the group C [(15.734 ± 4.987)μg/ml] was significantly higher in that in the group HS [(9.958 ± 4.283) μg/ml, <0.05)]. The results of HE staining and TEM showed that there was myocardium injury in the rats with heat stroke, which was milder in the groups VitE HS and Valsartan HS compared with the group HS. Conclusions Death mainly occurs in 24 hours after the onset and the major risk factors are low body temperature and long time of striking, but the relatively high rate of weight change is the protective factor of the rat survival. Myocardium injury exists in the rat model of heat stroke, the potential mechanism may be apoptosis of myocardial cells induced by oxidative stress and angiotensin Ⅱ.