Objective To explore the myocardial enzyme, histology and ultrastructure changes of heat stroke rats in dry-heat desert environment.Methods Forty-eight male SD rats were randomly divided into 6 groups: mild heat stroke group and its control group, moderate heat stroke group and its control group, severe heat stroke group and its control group. Then the three experimental groups of rats were put into dry-heat environment (temperature 41℃, humidity 10％) and the three control groups were put into normal environment (temperature 25℃, humidity 35%). After establishment of the heat stroke rat models, the rats were sacrificed at their corresponding time points (70, 110 and 145 min) from the beginning of the experiment for the mild heat stroke group and its control group, moderate heat stroke group and its control group, and severe heat stroke group and its control group, respectively. Blood samples were taken and heart tissues were harvested. The serum enzymes CK, CK-MB, and LDH were detected by an automatic biochemical analyzer. The pathological examination was performed with HE staining and ultrastructural changes were observed by electron microscopy. Results The serum enzymes CK, CK-MB, LDH were significantly higher in the dry-heat stroke groups than that in their control groups (P<0.05). The serum CK, CK-MB, LDH levels were increased along with the progression of heat stroke, of which, CK and LDH of the mild heat stroke group were significantly different compared with that of the moderate heat stroke group or severe heat stroke group (P<0.05). However, there were no significant difference between the moderate and severe heat stroke groups (P >0.05). CK-MB levels were significantly different between every two groups of the three heat stroke groups (P<0.05). The pathological examination showed dilation and congestion of blood vessels and hemorrhage, which became more serious along with the prolongation of exposure to dry-heat. The control group showed no abnormalities. Electron microscopy showed disruption of myofilaments and myolysis, blurred Z lines, swollen mitochondria, cytoplasmic vacuolization in the cardiomyocytes of heat stroke rats, and all these myocardial cell injuries became more serious along with the progression of heat-stroke. Conclusions Dry-heat desert environment can cause myocardial injury, and gradually getting worse along with the prolongation of dry-heat exposure and progression of heat stroke. Our findings suggest that attention should be paid to protection of the myocardium against injurious effect of heat stroke in dry-heat desert environment.