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Ultrafine ambient particulate matter enhances cardiac ischemia and reperfusion injury
Citation:
TONG, H., M. I. GILMOUR, J. M. SAMET, AND R. B. DEVLIN. Ultrafine ambient particulate matter enhances cardiac ischemia and reperfusion injury. Presented at American Thoracic Society Annual Meeting, San Diego, CA, May 15 - 20, 2009.
Impact/Purpose:
research results
Description:
Epidemiological studies have demonstrated a consistent link between exposure to ambient particulate air pollutant (PM) and the incidence of cardiovascular morbidity and mortality. The present study was designed to evaluate the cardiac effects of ambient PM. Mice were exposed to 100 g of ambient coarse, fine, and ultrafine particles, or saline by oropharyngeal instillation. Twenty-four hours later, cardiac damage was assessed by Langendorff-method of cardiac ischemia/perfusion. Mouse hearts were perfused for 25 min prior to 20 min of global ischemia followed by 2 hours of reperfusion. Recovery of post-ischemic left ventricular developed pressure (LVDP) and infarct size were measured at 1 and 2 hours of reperfusion, respectively. Coronary flow rate was measured before, during, and after ischemia. Hearts from ultrafine-exposed mice had significant lower cardiac functional recovery (24.0±10.2% for ultrafine vs. 53.2±3.9% for saline, p<0.05) and greater infarct size (63.4±7.0% for ultrafine vs. 44.4±5.8% for saline, p<0.05). Hearts from coarse and fine PM-exposed mice had lower recovery of cardiac function (34.4±8.5% for coarse and 32.6±9.5% for fine) and larger infarct size (52.8±7.5% for coarse and 49.6±3.5% for fine) than the saline hearts, but these effects were not statistically significant. The coronary flow rate was significantly decreased in the hearts of mice exposed to ultrafine PM (2.5±0.3 ml/min in the UF group vs. 3.7±0.5 ml/min in the saline group; p<0.05), but not in those obtained from animals treated with fine or coarse particles. In addition, exposure to ultrafine and fine PM resulted in a decrease in phospho-AKT level in the cardiac tissues. These results suggest that the enhanced cardiac ischemic/reperfusion injury provoked by ultrafine particles involves the inhibition of survival AKT signaling. The findings of this study provide evidence of particle size-dependent specificity in the adverse effects of PM exposure, with smaller particles promoted cardiovascular injury. This abstract of a proposed presentation does not necessarily reflect EPA policy.