流行病学显示，极热期间美国中暑发生率为20/10万人，潜在死亡率约40%，我国南方地区中暑死亡率达10～15%。湿热环境使人体各种生理功能减退，心血管系统是湿热应激时机体最先和最易受损伤的部位，但湿热应激心肌损伤的机制尚未明确,临床上缺乏特异性的治疗手段。课题组前期研究发现血管紧张素II、活性氧在湿热应激心脏损伤中有重要作用，拟通过建立湿热环境下心肌损伤模型，检测各项相关指标，进一步探究湿热应激心脏损伤的病理机制，明确血管紧张素II、NLRP3炎性小体、活性氧等在湿热应激致心肌损伤过程的作用机制，探寻AngII拮抗剂和抗氧化应激药物在湿热应激致心肌损伤中的保护作用，为临床治疗湿热应激心脏损伤提供理论基础。

Epidemiological data show that during extreme heat,the incidence of heat stroke in US is 20 per 100000,the potential mortality rate of them is about 40%,heat stroke mortality rate may be as high as 10-15% in South China.Hot and humid condition can cause a variety of human physiological hypofunction,while cardiovascular system is the first and most vulnerable to injury site, the mechanisms of myocardial injury induced by humid heat stress are not yet clear,the lack of specificity of clinical treatment.Our group undertakes to detect the relevant index through establishment of the proposed model under hot and humid environment,futher explore the pathogenesis of heart damage,clarify the mechanisms of angiotensin Ⅱ,NLRP3 inflammasome,reactive oxygen species(ROS) in the process of humid heat stress induced myocardical injury,research AngⅡ antagonist and anti-oxidative stress drugs in the heart,in order to provide a theoretical basis for clinical research and for the patients.