Objective To discuss the cardiac toxicities of a heat waves and ozone exposure on cardiovascular diseases（CVDs） and explore a possible mechanism. Methods The incidence of ozone exposure combined with heat wave was s...Objective To discuss the cardiac toxicities of a heat waves and ozone exposure on cardiovascular diseases（CVDs） and explore a possible mechanism. Methods The incidence of ozone exposure combined with heat wave was simulated in the Shanghai Meteorological and Environmental Animal Exposure System（Shanghai-METAS）. A total of 64 Apo E-/-mice, matched by weight, were randomly divided into 8 groups and exposed to heat wave conditions or ozone. The levels of creatine kinase（CK）, D-lactate dehydrogenase（D-LDH）, intercellular adhesion molecule 1（sICAM-1）, tumor necrosis factor alpha（TNF-α）, nitric oxide（NO）, endothelin-1（ET-1）, D-dimer（D2 D）, plasminogen activator inhibitor-1（PAI-1） and blood lipid in plasma and heat shock protein-60（HSP60）, hypoxia inducible factor 1 alpha（HIF-1α）, interleukin-6（IL-6）, C-reactive protein（CRP）, superoxide dismutase（SOD）, and malondialdehyde（MDA） in hearts were measured after exposure. Results The levels of all indicators, except for SOD, increased with the ozone-only exposure. However, cardiac damage was most significant when the heat wave conditions were combined with severe ozone exposure. Moreover, the levels of CK, D-LDH, NO, PAI-1, sICAM-1, and TNF-α in plasma increased significantly（P 〈 0.05）, and the contents of HSP60, HIF-1α, CRP, and MDA in hearts increased considerably（P 〈 0.05）, but the activity of SOD decreased significantly. In addition, the levels of four blood lipid items remarkably increased（except the level of HDL-C which decreased significantly） with ozone exposure. Conclusion A short-term exposure to a heat wave and ozone causes severe toxic effects on the heart. Cardiac damage was most significant under combined heat wave and severe ozone exposure simulations.展开更多
基金supported by the National Natural Science Foundation of China [Grant No.41375121]the Key Research Plan of Hebei Province,China [Grant No.18273705D]
文摘Objective To discuss the cardiac toxicities of a heat waves and ozone exposure on cardiovascular diseases（CVDs） and explore a possible mechanism. Methods The incidence of ozone exposure combined with heat wave was simulated in the Shanghai Meteorological and Environmental Animal Exposure System（Shanghai-METAS）. A total of 64 Apo E-/-mice, matched by weight, were randomly divided into 8 groups and exposed to heat wave conditions or ozone. The levels of creatine kinase（CK）, D-lactate dehydrogenase（D-LDH）, intercellular adhesion molecule 1（sICAM-1）, tumor necrosis factor alpha（TNF-α）, nitric oxide（NO）, endothelin-1（ET-1）, D-dimer（D2 D）, plasminogen activator inhibitor-1（PAI-1） and blood lipid in plasma and heat shock protein-60（HSP60）, hypoxia inducible factor 1 alpha（HIF-1α）, interleukin-6（IL-6）, C-reactive protein（CRP）, superoxide dismutase（SOD）, and malondialdehyde（MDA） in hearts were measured after exposure. Results The levels of all indicators, except for SOD, increased with the ozone-only exposure. However, cardiac damage was most significant when the heat wave conditions were combined with severe ozone exposure. Moreover, the levels of CK, D-LDH, NO, PAI-1, sICAM-1, and TNF-α in plasma increased significantly（P 〈 0.05）, and the contents of HSP60, HIF-1α, CRP, and MDA in hearts increased considerably（P 〈 0.05）, but the activity of SOD decreased significantly. In addition, the levels of four blood lipid items remarkably increased（except the level of HDL-C which decreased significantly） with ozone exposure. Conclusion A short-term exposure to a heat wave and ozone causes severe toxic effects on the heart. Cardiac damage was most significant under combined heat wave and severe ozone exposure simulations.
