论文部分内容阅读
目的 探讨高温高湿环境对大鼠胸主动脉血管功能的影响及其可能机制,为防控炎热环境下心血管疾病的发病提供科学的理论依据.方法 将正常对照大鼠(Wistar kyoto rats,WKY)和自发性高血压大鼠(spontaneously hypertensive rats,SHR)各24只,按每天热应激时间的不同随机分为6组,分别为WKY对照组、热应激8h组、热应激24 h组及SHR对照组、热应激8h组、热应激24 h组,每组8只.对照组室温为24℃,热应激组室温为32℃,热应激时间为1周.热应激前后分别测定各组大鼠血压;热应激结束后,用20％乌拉坦(1 ml/100 g)麻醉大鼠,分离大鼠胸主动脉血管,采用器官浴槽测定胸主动脉血管环对去甲肾上腺素的反应性;采用RT-PCR法检测大鼠胸主动脉血管组织凋亡基因caspase-3、Bcl-2、Bax的mRNA表达量;采用Western-blot方法检测胸主动脉血管组织凋亡蛋白Bcl-2和Bax蛋白水平的变化.结果 与热应激前比较,SHR热应激8h和24 h组大鼠的收缩压和舒张压均明显升高,差异有统计学意义(P＜0.05或P＜0.05).与WKY大鼠比较,SHR大鼠的胸主动脉血管反应性升高,差异有统计学意义(P＜0.05).高温高湿环境可使大鼠胸主动脉caspase-3 mRNA表达量升高,BcI-2mRNA表达量降低,Bax mRNA表达量升高,差异均有统计学意义(P＜0.05).SHR热应激8h和24 h组大鼠的Bax mRNA表达量高于SHR对照组,差异有统计学意义(P＜0.01).结论 高温高湿环境对大鼠胸主动脉血管有一定的损伤,这些损伤作用可能与机体适应程度及细胞凋亡机制有关.“,”Objective To understand the mechanism of high temperature and humidity (heat stress) on the functions of blood vessels of the rats and to provide the scientific basis for the prevention and control of cardiovascular disease in the hot environment.Methods A total of 24 normal control rats (Wistar-Kyoko Rats,WKY) and 24 spontaneously hypertensive rats (SHR) were randomly divided into six groups,eight in each,WKY control group (WKY-CN),WKY 8 h-heat stress group (WKY-8),WKY 24 h-heat stress group (WKY-24),SHR control group (SHR-CN),SHR 8 h-heat stress group (SHR-8),SHR 24 h-heat stress group (SHR-24),respectively.The room temperature for the control group was 24 ℃,while for the heat stress group was 32 ℃,heat stress period was one week.The blood pressure was measured before and after heat stress.After heat stress,all rats were anesthetized with 20％ urethane (1 ml/100 mg).The thoracic aorta was isolated and norepinephrine (NE) reactivity of thoracic aorta was measured by using organ bath.RT-PCR was used to detect the expression of caspase-3,Bcl-2 and Bax mRNA in the thoracic aorta of rat,while Western-blot was used to detect the changes of Bcl-2 and Bax protein levels.Results Compared with the control,the systolic and diastolic blood pressure of rats increased significantly after heat stress in the SHR-8 and SHR-24 groups (P＜0.01,P＜0.05).Compared with the WKY rats,the heat stress promoted significantly NE reactivity of thoracic aorta in SHR rats (P＜0.05) and induced up-regulated expression of caspase-3,Bax mRNA and downregulated expression of Bcl-2 mRNA (P＜0.05) in SHR rats.Caspase-3 and Bax gene expression were increased in SHR rats after heat stress (P＜0.01).Conclusion The heat stress may cause injury in the thoracic aorta of rats through its apoptotic effects and the damage may be associated with the body adaption degree and the mechanism of apoptosis.