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目的观察高温应激对大鼠心肌血管紧张素Ⅱ(AngⅡ)的影响,探讨心肌AngⅡ与心肌p22phox表达的关系。方法将24只成年雄性SD大鼠,随机分为:对照组、高温组、高温高湿组,每组8只。喂养4周后,颈动脉插管测定平均动脉压。用放射免疫法测定血浆和心肌AngⅡ浓度。用比色法测定心肌活性氧(ROS)水平。应用逆转录聚合酶链式反应(RT-PCR)和免疫组化法检测心肌p22phox mRNA及蛋白的表达水平。结果高温组和高温高湿组大鼠平均动脉压、AngⅡ浓度、ROS水平、p22phox mRNA及蛋白的表达水平与对照组比较,均有显著升高(P<0.01);高温高湿组与高温组比较,无显著性差异。结论高温应激使大鼠血压升高,这可能与AngⅡ水平上调有关。AngⅡ介导ROS生成增加,其机制可能是高温应激引起p22phox超常表达所致,提示高温应激可引起心脏损害。
Objective To investigate the effect of high temperature stress on myocardial angiotensin Ⅱ (Ang Ⅱ) in rats and to explore the relationship between myocardial Ang Ⅱ and myocardial p22phox expression. Methods Twenty-four adult male Sprague-Dawley rats were randomly divided into control group, high temperature group and high temperature and high humidity group, with 8 rats in each group. After 4 weeks of feeding, mean arterial pressure was measured by carotid cannulation. Plasma and myocardial Ang Ⅱ concentrations were measured by radioimmunoassay. Myocardial reactive oxygen species (ROS) levels were measured by colorimetry. Reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry were used to detect the expression of p22phox mRNA and protein in myocardium. Results Compared with the control group, the mean arterial pressure, Ang Ⅱ concentration, ROS level and the expression of p22phox mRNA and protein of the rats in high temperature and high temperature and high humidity groups were significantly increased (P <0.01). Compared with the high temperature and high humidity group Comparison, no significant difference. Conclusion High temperature stress can increase the blood pressure of rats, which may be related to the up-regulation of AngⅡ. AngⅡ-mediated ROS generation increased, the mechanism may be caused by hyperthermia caused by p22phox overexpression, suggesting that high-temperature stress can cause heart damage.