RESUMO
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 ApoE-/- 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 (D2D), 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.