Effects of simulated heat waves on cardiovascular functions in senile mice.

Xiakun Zhang,Shuyu Zhang,Lina Dong,Pinwen Guo,Jing Lu,Chunling Wang,Baojian Wang

doi:10.3390/ijerph110807841

Abstract

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.

Highlights

Human health is related to the weather
Previous studies [37,38] indicated that excessive heat shock protein 60 (HSP60) in myocardium can activate immune cells, induce endothelial cells and macrophages to secrete a large amount of ICAM-1, tumor necrosis factor (TNF)-α, and other inflammatory cytokines
This experiment showed that high temperature can elevate the HSP60 expression levels in myocardium of senile mice, which can accelerate atherosclerosis, and result in the occurring and development of coronary heart disease (CHD); the BH4 can decrease HSP60 expression levels in myocardium of senile mice, thereby it can relieve the effect of heat waves on coronary artery of senile mice; heat wave exposure induces the increment of the secretion of cytokines TNF and soluble intercellular adhesion molecule (sICAM)-1 in senile mice, while for the senile mice group that added BH4, they are less subjected to the heat waves with obvious lower TNF and sICAM-1compared with the heat waves group

Summary

Introduction

Human health is related to the weather. The frequent occurrence of extreme weather in recent years has brought economic losses and endangered human health [1]. Epidemiological studies and statistical studies have demonstrated that heat waves significantly increase the incidence of coronary heart disease (CHD), and many people are admitted to hospitals or die because of heat exposure during heat waves [2]. Kunst et al [3] studied the relationship between extreme weather and mortality from 1979 to. 1987, and found that 26% of heat-induced deaths were caused by cardiovascular diseases. Found that the incidence rate of cardiovascular disease is 35.1% of the total number during hot weather, including the CHD incidence rate of 10.8%. The China Cardiovascular Report [5] showed that about

Results

Discussion

Conclusion