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Ultrafine particulate matter (UFP) has been associated with increased cardiovascular morbidity and mortality. However, the mechanisms that drive PM-associated cardiovascular disease and dysfunction remain unclear. We examined the impact of oropharyngeal aspiration of 100 μg UFP from the Chapel Hill, NC, air shed in Sprague-Dawley rats on cardiac function, arrhythmogenesis, and cardiac ischemia/reperfusion (I/R) injury using a Langendorff working heart model. We found that exposure to UFP was capable of significantly exacerbating cardiac I/R injury without changing overall cardiac function or major changes in arrhythmogenesis. Cardiac I/R injury was attenuable with administration of cyclosporin A (CsA), suggesting a role for the mitochondrial permeability transition pore (mPTP) in UFP-associated cardiovascular toxicity. Isolated cardiac mitochondria displayed decreased Ca 2+ buffering before opening of the mPTP. These findings suggest that UFP-induced expansion of cardiac I/R injury may be a result of mPTP Ca 2+ sensitization resulting in increased mitochondrial permeability transition and potential initiation of mPTP-associated cell death pathways.

Ultrafine Particulate Matter Increases Cardiac Ischemia/Reperfusion Injury via Mitochondrial Permeability Transition Pore