Diesel exhaust inhalation causes vascular dysfunction and impaired endogenous fibrinolysis

Article

关键词: PARTICULATE AIR-POLLUTION;    ENDOTHELIAL DYSFUNCTION;    CIGARETTE-SMOKING;    OXIDATIVE STRESS;    DAILY MORTALITY;    TERM EXPOSURE;    PARTICLES;    ASSOCIATION;   

DOI  :  10.1161/CIRCULATIONAHA.105.588962

来源: SCIE

【 摘 要 】

Background - Although the mechanisms are unknown, it has been suggested that transient exposure to traffic-derived air pollution may be a trigger for acute myocardial infarction. The study aim was to investigate the effects of diesel exhaust inhalation on vascular and endothelial function in humans. Methods and Results - In a double-blind, randomized, cross-over study, 30 healthy men were exposed to diluted diesel exhaust (300 mu g/m(3) particulate concentration) or air for 1 hour during intermittent exercise. Bilateral forearm blood flow and inflammatory factors were measured before and during unilateral intrabrachial bradykinin ( 100 to 1000 pmol/min), acetylcholine (5 to 20 mu g/min), sodium nitroprusside (2 to 8 mu g/min), and verapamil (10 to 100 mu g/min) infusions 2 and 6 hours after exposure. There were no differences in resting forearm blood flow or inflammatory markers after exposure to diesel exhaust or air. Although there was a dose-dependent increase in blood flow with each vasodilator ( P < 0.0001 for all), this response was attenuated with bradykinin ( P < 0.05), acetylcholine ( P < 0.05), and sodium nitroprusside ( P < 0.001) infusions 2 hours after exposure to diesel exhaust, which persisted at 6 hours. Bradykinin caused a dose-dependent increase in plasma tissue plasminogen activator ( P < 0.0001) that was suppressed 6 hours after exposure to diesel ( P < 0.001; area under the curve decreased by 34%). Conclusions - At levels encountered in an urban environment, inhalation of dilute diesel exhaust impairs 2 important and complementary aspects of vascular function in humans: the regulation of vascular tone and endogenous fibrinolysis. These important findings provide a potential mechanism that links air pollution to the pathogenesis of atherothrombosis and acute myocardial infarction.

【 授权许可】

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