Comparison on myocardial injury in rats with classic versus exertional heat stroke

Abstract

Objective To compare the differences in myocardial injury in rat models of exertional heat stroke (EHS) and classic heat stroke (CHS) in order to provide possible laboratory basis for clinical treatment of heat stroke. Methods A total of 80 SD rats were randomly divided into control group (n=10), exercise group (EXC, n=10), classic heat stroke group (CHS, n=30) and exertional heat stroke group (EHS, n=30). The rats in the control and EXC groups were exposed to a condition of ambient temperature of (25±0.5) ℃ and relative humidity of (50±5)%, and those of the EHS and CHS groups were placed in a simulated hot climate chamber with an ambient temperature of (39.0±0.5) ℃ and a relative humidity of (50±5)%. The rats in the EHS and EXC groups were administered to treadmill exercise treatment under a running speed of 12 m/min and a slope of 0°, and rested for 2 min in every 8 min of exercise to monitor rectal temperature. When the core body temperature reached 42.3 ℃ or collapsed (tail pinching reflex disappeared), the rats were taken to normal temperature and rewarmed. Echocardiography was used to detect the cardiac function, and serum myocardial enzymes (AST, LDH, CK-MB and CK) were detected by biochemical analyzer. HE staining was used to detect the pathological changes of rat myocardial tissue. The apoptosis of cardiomyocytes was detected by TUNEL staining. The expression levels of quinone oxidoreductase 1 (Nrf2), cleaved Caspase-3, anti-apoptotic protein (Bcl-2), pro-apoptotic protein (Bax) and heme oxygenase-1 (HO-1) were detected by Western blotting. Results Compared with the CHS group, the EHS group had significantly shortened latent period (P 0.05). Echocardiography indicated that statistically lower left ventricular ejection fraction (LVEF) (P < 0.05) and higher AST and LDH levels (P < 0.01) were observed in the EHS group than the CHS group. The pathological changes of acute myocardial injury including myocardial cell edema, disordered and broken muscle fibers, and inflammatory infiltration, were observed in both groups, but the pathological score of myocardial injury was notably higher in the EHS group than the CHS group (P < 0.05), so was the apoptotic rate of cardiomyocytes (P < 0.05). The protein levels of oxidative stress-related signaling pathway-related proteins were significantly higher in the EHS group than the CHS group. Conclusion High ambient temperature combined with exercise has a higher susceptibility to heat stroke. EHS-mediated abnormal cardiac dysfunction and myocardial apoptosis were more severe than CHS inducement, which may be related to the activation of oxidative stress-related signaling pathways.

Keywords

• classic heat stroke
• exertional heat stroke
• cardiac injury
• echocardiography
• apoptosis