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Ultrafine particulate matter exposure augments ischemia-reperfusion injury in mice

Departments of ¹Physiology and ²Internal Medicine Cardiology Division, Brody School of Medicine at East Carolina University, Greenville; and ³National Health and Environmental Effects Research Laboratory, Environmental Protection Agency, Research Triangle Park, North Carolina

Submitted 22 December 2005 ; accepted in final form 27 March 2006

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 µm) PM exposure on ischemia-reperfusion (I/R) injury. ICR mice were exposed to 100 µg of PM or vehicle by intratracheal instillation. Twenty-four hours later, mice were anesthetized with pentobarbital sodium (60 mg/kg), the left anterior descending coronary artery was ligated for 20 min, flow was restored for 2 h, and the resulting myocardial infarct (MI) size was evaluated. PM exposure doubled the relative size of the MI compared with the vehicle control. No difference was observed in the percentage of the left ventricle at risk for ischemia. PM exposure increased the level of oxidative stress in the myocardium after I/R. The density of neutrophils in the reperfused 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 h after PM exposure could not be correlated to the increased I/R injury observed. Additionally, aortas isolated from PM-exposed animals and studied in vitro exhibited a reduced endothelium-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 I/R in a murine model.

myocardial infarction; vascular reactivity; oxidant injury; acetylcholine

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