You are here:
ULTRAFINE PARTICULATE MATTER EXPOSURE AUGMENTS ISCHEMIA REPERFUSION INJURY IN MICE
Citation:
COZZIE, D., S. HAZARIKA, H. W. STALLINGS, R. LUST, C. WINGARD, M. R. VAN SCOTT, W. CASCIO, AND R. B. DEVLIN. ULTRAFINE PARTICULATE MATTER EXPOSURE AUGMENTS ISCHEMIA REPERFUSION INJURY IN MICE. Presented at Federation of American Societies for Experimental Biology Annual Meeting, San Francisco, CA, April 01 - 05, 2006.
Description:
Epidemiological studies have linked ambient particulate matter (PM) levels to an increased incidence of adverse cardiovascular events. Yet little is definitively known about the mechanisms accounting for the cardiovascular events associated with PM-exposure. The goal of this study was to determine the effects of ultrafine (<0.1 m) PM-exposure on ischemia reperfusion (IR) injury. Mice were exposed to 100 g of PM or Vehicle by tracheal instillation. Twenty four hours later, the left anterior descending coronary artery (LAD) was ligated for 20 minutes, flow was restored for 2 hours, and the resulting myocardial infarct (MI) size was evaluated. PM-exposure doubled the relative size of the MI compared to the Vehicle control. No difference was observed in the size
of the area at risk (AAR). PM-exposure increased the level of oxidative stress in the myocardium after ischemia and reperfusion. The density of neutrophils in the myocardium was increased by PM-exposure, but differences in the number of blood leukocytes, expression of adhesion molecules on circulating neutrophils, and activation state of circulating neutrophils 24 hours after PM-exposure could not be correlated to the increased IR injury observed. Additionally, aortas isolated from PM-exposed animals and studied in vitro exhibited a reduced endothelial-dependent relaxation response to acetylcholine. These results indicate that exposure to ultrafine PM increases oxidative stress in the myocardium, alters vascular reactivity, and augments injury after IR.