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Am J Physiol Heart Circ Physiol (March 31, 2006). doi:10.1152/ajpheart.01362.2005
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Submitted on December 22, 2005
Accepted on March 27, 2006

Ultrafine particulate matter exposure augments ischemia reperfusion injury in mice

Emily Cozzi1, Surovi Hazarika1, Howard W Stallings, III1, Wayne E Cascio2, Robert B Devlin3, Robert M Lust1, Christopher J Wingard1, and Michael R Van Scott1*

1 Physiology, Brody School of Medicine at ECU, Greenville, North Carolina, United States
2 Internal Medicine, Division of Cardiology, Brody School of Medicine, North Carolina, United States
3 National Health and Environmental Effects Research Laboratory, EPA, Research Triangle Park, North Carolina, United States

* To whom correspondence should be addressed. E-mail: vanscottmi{at}ecu.edu.

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 (<0.1µm) PM- exposure on ischemia reperfusion (IR) injury. ICR mice were exposed to 100µg of PM or Vehicle by intratracheal instillation. Twenty four hours later mice were anesthetized with sodium pentobarbital (60mg/kg), the left anterior descending coronary artery 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 percentage of the left ventricle at risk for ischemia. PM-exposure increased the level of oxidative stress in the myocardium after ischemia and reperfusion. 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 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 in a murine model.




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