| Objective: To explore myocardial injury effects on heat stroke rats in dry-heat desert environment,andprovide evidence for the prevention and treatment of heat stroke organism myocardial injury in dry-heatdesert environment.Methods: Forty-eight male SD rats were randomly divided into6groups: mild heat stroke group and itscontrol group,moderate heat stroke group and its control group,severe heat stroke group and its controlgroup.Then the three experimental groups of rats were put into dry-heat environment (temperature41℃,humidity10%)and the three control groups were put into normal environment (temperature25℃,humidity35%).After establishment of the heat stroke rat models,the rats were sacrificed at their corresponding timepoints (70,110and145min) from the beginning of the experiment for the mild heat stroke group and itscontrol group,moderate heat stroke group and its control group,and severe heat stroke group and its controlgroup,respectively. Blood samples were taken and heart tissues were harvested.The serum enzymesCK,CK-MB,and LDH were detected by an automatic biochemical analyzer.Serum cytokine TNF-α and IL-1β by ELISA method. The pathological examination was performed with HE staining and ultrastructuralchanges were observed by electron microscopy.Results: The serum enzymes CK,CK-MB,LDH were significantly higher in the dry-heat stroke groups thanthat in their control groups (P <0.05).The serum CK,CK-MB,LDH levels were increased along with theprogression of heat stroke,of which,CK and LDH of the mild heat stroke group were significantly differentcompared 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).TNF-α and IL-1β test results: The serum TNF-α,IL-1βwere significantly higher in the dry-heatstroke groups than that in their control groups (P <0.01),of which,TNF-α and IL-1β of the mild heatstroke group were significantly different compared with that of the moderate heat stroke group or severeheat stroke group (P <0.01).The pathological examination showed dilation and congestion of blood vesselsand hemorrhage,which became more serious along with the prolongation of exposure to dry-heat.Thecontrol group showed no abnormalities. Electron microscopy showed disruption of myofilaments andmyolysis, blurred Z lines,swollen mitochondria,cytoplasmic vacuolization in the cardiomyocytes of heatstroke rats,and all these myocardial cell injuries became more serious along with the progression ofheat-stroke.The myocardial apoptosis results: The myocardial apoptosis index were significantly higher inthe dry-heat stroke groups than that in their control groups (P <0.05).Difference was statisticallysignificant compared with every group in dry heat stroke (P <0.01),and increased along with theprogression of heat stroke.Conclusions: Dry-heat desert environment can cause myocardial injury,and gradually getting worse alongwith the prolongation of dry-heat exposure and progression of heat stroke. Our findings suggest thatattention should be paid to protection of the myocardium against injurious effect of heat stroke in dry-heat desert environment.... |