中文摘要：

[目的]观察高温环境对大鼠心功能的损伤作用并探讨其机制。[方法]选择清洁级SD雄性大鼠30只,随机分为2组,分别为常温对照组和热损伤组。常温对照组大鼠置于室温。将热损伤组大鼠麻醉并行股动脉和左心室插管术后,暴露于42℃热循环舱中,持续75 min,实时监测体核温度（Tc）、平均动脉压（MAP）、心率（HR）、动脉收缩压（SAP）、动脉舒张压（DAP）、左室收缩压峰值（LVSP）、左室舒张末期压（LVEDP）及左心室等容收缩期压力变化最大速率（±dp/dt）。动物热损伤后迅速取出,采血,检测大鼠血清谷草转氨酶（AST）、碱性磷酸酶（ALP）、乳酸脱氢酶（LDH）、磷酸肌酸激酶（CK）水平;常规苏木素-伊红染色,观察心肌组织病理改变。[结果]在热损伤30 min后,热损伤组大鼠Tc、MAP、HR,SAP、DAP、LVSP、LVEDP、±dp/dt与常温对照组比较均有所升高（均P〈0.05）;75 min时,除Tc、LVEDP保持在较高水平外,其他各指标均有所降低。热损伤组大鼠AST、ALP、LDH及CK水平分别为（147.29±15.31）U/L、（379.79±35.25）U/L、（2276.07±245.41）U/L及（748.07±81.17）U/L,明显高于常温对照组（均P〈0.05）。[结论]高温环境对大鼠心功能具有损伤作用,此损伤作用与高温环境导致动脉血压改变和心肌组织缺血缺氧有关。

英文摘要：

[Objective] To investigate whether cardiac injury to rat is induced by high temperature environment and study associated mechanism.[Methods] Thirty male SD rats of clean degree were randomly divided into normothermic control group（n=15） and heat injury group（n=15）.The heat injury group rats were exposed to heat（42℃ for 75 min） after anesthesia and femoral artery/left ventricular catheterization,and the normal control group rats were kept at room temperature.Real-time monitoring data were collected for core body temperature（Tc）,mean arterial pressure（MAP）,heart rate（HR）,systolic arterial blood pressure（SAP）,diastolic artery pressure（DAP）,left ventricular peak systolic pressure（LVSP）,left ventricular end-diastolic pressure（LVEDP）,and left ventricular isovolumetric systolic pressure change rate（±dp/dt）.After thermal damage was induced,blood samples were collected immediately to detect rats’ serum aspartate aminotransferase（AST）,alkaline phosphatase（ALP）,lactate dehydrogenase（LDH）,and creatine phosphate kinase（CK） levels.Observing heart tissue pathological changes was also carried out using hematoxylin and eosin stain.[Results] Compared with the normothermic controls,all heat injury rats’ Tc,MAP,HR,SAP,DAP,LVSP,LVEDP,and ±dp/dt were higher after 30 min in the designed high temperature environment（all Ps 〈 0.05）.After 75 min,the Tc and LVEDP remained at a high level,while other indicators were reduced.The levels of AST,ALP,LDH,and CK of the heat injury model group were（147.29±15.31）U/L,（379.79±35.25）U/L,（2276.07±245.41）U/L,and（748.07±81.17）U/L,respectively,and were significantly higher than those of the normal control group（all Ps 〈 0.05）.[Conclusion] High temperature environment could result in the change of arterial blood pressure and myocardial tissue ischemia hypoxia in rats,indicating cardiac dysfunction.