Zhang Xiakun, Lu Jing, Zhang Shuyu, Wang Chunling, Wang Baojian, Guo Pinwen, Dong Lina
School of Atmospheric Science, Nanjing University of Information Science and Technology, 219 Ningliu Road, Nanjing 210044, China.
Computer Science Department, Oklahoma State University, 219 MSCS, Stillwater, OK 74078, USA.
Int J Environ Res Public Health. 2014 Aug 6;11(8):7841-55. doi: 10.3390/ijerph110807841.
The mechanism of the effects of simulated heat waves on cardiovascular disease in senile mice was investigated. Heat waves were simulated in a TEM1880 meteorological environment simulation chamber, according to a heat wave that occurred in July 2001 in Nanjing, China. Eighteen senile mice were divided into control, heat wave, and heat wave BH4 groups, respectively. Mice in the heat wave and heat wave BH4 groups were exposed to simulated heat waves in the simulation chamber. The levels of ET-1, NO, HSP60, SOD, TNF, sICAM-1, and HIF-1α in each group of mice were measured after heat wave simulation. Results show that heat waves decreased SOD activity in the myocardial tissue of senile mice, increased NO, HSP60, TNF, sICAM-1, and HIF-1α levels, and slightly decreased ET-1 levels, BH4 can relieve the effects of heat waves on various biological indicators. After a comprehensive analysis of the experiments above, we draw the followings conclusions regarding the influence of heat waves on senile mice: excess HSP60 activated immune cells, and induced endothelial cells and macrophages to secrete large amounts of ICAM-1, TNF-α, and other inflammatory cytokines, it also activated the inflammation response in the body and damaged the coronary endothelial cell structure, which increased the permeability of blood vessel intima and decreased SOD activity in cardiac tissues. The oxidation of lipoproteins in the blood increased, and large amounts of cholesterol were generated. Cholesterol penetrated the intima and deposited on the blood vessel wall, forming atherosclerosis and leading to the occurrence of cardiovascular disease in senile mice. These results maybe are useful for studying the effects of heat waves on elderly humans, which we discussed in the discussion chapter.
研究了模拟热浪对老年小鼠心血管疾病的影响机制。根据2001年7月在中国南京发生的一次热浪，在TEM1880气象环境模拟舱中模拟热浪。18只老年小鼠分别分为对照组、热浪组和热浪BH4组。热浪组和热浪BH4组的小鼠在模拟舱中暴露于模拟热浪。在热浪模拟后，测量每组小鼠的ET-1、NO、HSP60、SOD、TNF、sICAM-1和HIF-1α水平。结果表明，热浪降低了老年小鼠心肌组织中的SOD活性，增加了NO、HSP60、TNF、sICAM-1和HIF-1α水平，并略微降低了ET-1水平，BH4可以缓解热浪对各种生物学指标的影响。在对上述实验进行综合分析后，我们得出了关于热浪对老年小鼠影响的以下结论：过量的HSP60激活免疫细胞，诱导内皮细胞和巨噬细胞分泌大量ICAM-1、TNF-α等炎性细胞因子，还激活体内炎症反应并破坏冠状动脉内皮细胞结构，增加血管内膜通透性并降低心脏组织中的SOD活性。血液中脂蛋白氧化增加，产生大量胆固醇。胆固醇穿透内膜并沉积在血管壁上，形成动脉粥样硬化并导致老年小鼠发生心血管疾病。这些结果可能有助于研究热浪对老年人的影响，我们将在讨论章节中进行讨论。
