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.