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Effects of Simulated Heat Waves on Cardiovascular Functions in Senile Mice
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 divid...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4143836/ https://www.ncbi.nlm.nih.gov/pubmed/25101768 http://dx.doi.org/10.3390/ijerph110807841 |
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author | Zhang, Xiakun Lu, Jing Zhang, Shuyu Wang, Chunling Wang, Baojian Guo, Pinwen Dong, Lina |
author_facet | Zhang, Xiakun Lu, Jing Zhang, Shuyu Wang, Chunling Wang, Baojian Guo, Pinwen Dong, Lina |
author_sort | Zhang, Xiakun |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-4143836 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-41438362014-08-26 Effects of Simulated Heat Waves on Cardiovascular Functions in Senile Mice Zhang, Xiakun Lu, Jing Zhang, Shuyu Wang, Chunling Wang, Baojian Guo, Pinwen Dong, Lina Int J Environ Res Public Health Article 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. MDPI 2014-08-06 2014-08 /pmc/articles/PMC4143836/ /pubmed/25101768 http://dx.doi.org/10.3390/ijerph110807841 Text en © 2014 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/). |
spellingShingle | Article Zhang, Xiakun Lu, Jing Zhang, Shuyu Wang, Chunling Wang, Baojian Guo, Pinwen Dong, Lina Effects of Simulated Heat Waves on Cardiovascular Functions in Senile Mice |
title | Effects of Simulated Heat Waves on Cardiovascular Functions in Senile Mice |
title_full | Effects of Simulated Heat Waves on Cardiovascular Functions in Senile Mice |
title_fullStr | Effects of Simulated Heat Waves on Cardiovascular Functions in Senile Mice |
title_full_unstemmed | Effects of Simulated Heat Waves on Cardiovascular Functions in Senile Mice |
title_short | Effects of Simulated Heat Waves on Cardiovascular Functions in Senile Mice |
title_sort | effects of simulated heat waves on cardiovascular functions in senile mice |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4143836/ https://www.ncbi.nlm.nih.gov/pubmed/25101768 http://dx.doi.org/10.3390/ijerph110807841 |
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