Acute cardiac dysfunction after short-term diesel exhaust particles exposure.

Epidemiological studies show an association between particulate matter exposure and acute heart failure. However, underlying mechanisms remain unclear. In this study, we investigated acute cardiac hemodynamic effects and related mechanisms after 1 day exposure to diesel exhaust particles (DEPs). Male Sprague-Dawley rats were randomized and instilled with 250 microg (low dose) or 500 microg (high dose) of DEP or saline placebo intra-tracheally. The cardiac systolic function by dP/dt(40) and diastolic functions by maximal negative dP/dt were both worse in DEP low dose and DEP high dose groups than the control group, respectively. In the heart rate variability analysis, SDNN in DEP low dose and DEP high dose groups were both lower than the control group. The low frequency heart rate variability was higher in the DEP groups compared to the control group. The cardiac IL-1beta expression and circulating cardiac troponin I level were higher in the DEP group than the control group. Plasma IL-1beta and IL-6 protein were significantly higher in the DEP groups than the control group. In conclusion, DEP exposure causes acute cardiac systolic and diastolic dysfunction. The changes may be related to decreased heart rate variability, increased cardiac inflammatory reaction and myocardial damage.