| Objective To investigate protective effects of heat stress preconditioning on the heatstroke in rats and the mechanism of signal transduction about heat stress preconditioning.Methods The experiment consisted of two parts. The first part:the establishment of protective heat stress preconditioning model and investigation of effects of signal transduction pathway. This part included two experiments:1. Protective effects of heat stress preconditioning(42C,15min) on heatstroke in rats. 30 SD male rats were randomly divided into 3 groups:heat stress preconditioning group(42C,15min,HS group),sham heat stress control group(without heat stress preconditioning,SC group) and normal temperature control group(NC group). Three groups recovered for 20h at room temperature. Then all groups exposed to death in thermal environment(Td 39.5+0.5C,Tw 34.0+0.5C,relative humidity 65+3%). The existent time(interval between onset of heat stress and death),survival rate,the rectal temperatrue(Tr),heart rate(HR),mean arterial pressure(MAP) were measured continuously during heat exposure. The cerebral cortex,heart and liver were removed at the end of the experiment for detection of MDA and HSP70;2.1nvestigation of signal transduction pathway after heat stress preconditioning. 32 SD male rats were randomly divided into 4 groups:HS group,SC group,NC group and protein kinase C inhibitor group(inject protein kinase C inhibitor-chelerythrine chloride into rats' abdominal cavity lOmin before heat stress preconditioning,PKC group). Four groups recovered for 20h at room temperature. Then all groups exposed in thermal environment(Td 39.5+0.5C,Tw 34.0+0.5C,relative humidity 65 + 3%) for 73 min. The physiological index were measured continuously. The cerebral cortex,serum and heart were removed at the end of the experiment for detection of MDA and NO. The second part:Investigation of themechanism of signal transduction during establishment of protective heat stress preconditioning model. This part included two experiments:1. Study of tumor necrosis factor(TNF) and NO in PKC signal transduction pathway after heat stress preconditioning. 66 SD male rats were randomly divided into Oh group,2h group,4h group,8h group,12h group,24h group and control groups of each time point. The serum were separated and the concentration of TNF and NO were measured between Oh and 24h after heat stress preconditioning respectively. 2. Influence of PKC signal transduction pathway on the expression of HSP72 during establishment of the model. 24 SD male rats were randomly divided into 3 groups:HS group,NC group and PKC group. All groups recovered for 20h at room temperature. Then HSP72 of the cerebral cortex and myocardium were detection.Results The first part:1. Compared with SC group,existent time and survival rate increased significantly in HS group after heat exposure. MAP and HR were higher,but Tr was lower in HS group after heatstroke. At the end of experiments the content of MDA and HSP70 in the cerebral cortex and liver increased significantly vs SC group. 2. Compared with SC group,MAP,HR were higher,but Tr and MDA,NO in cerebral cortex,myocardium and serum was lower in HS group. Compared with HS group,the content of MDA and NO in the cerebral cortex,serum and myocardium increased significantly in PKC group,however MAP and HR was lower. The second part:1. The concentration of TNF reached the peak 4h after hat stress preconditioning. The concentration of NO amounted to peak 8h after hat stress preconditioning. 2. compared with NC group,the content of HSP72 in cerebral cortex and myocardium increased significantly in HS group. After application of chelerythrine chloride(a potent,selective PKC inhibitor),the content of HSP72 in cerebral cortex and myocardium decreased significantly compared with HS group.Conclusion 1. Heat stress preconditioning(42C,15min) delayed theheatstroke,enhanced thermotolerance and decreased death rate after heatstroke,which filled up the vacancy in China. 2. Heat stress preconditioning could enhance heart reserve and...
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