Diesel particulate matter exposure deteriorates cardiovascular health and increases the sensitivity of rat heart towards ischemia reperfusion injury via suppressing mitochondrial bioenergetics function.

Documents from previous studies do not sufficiently explain the pathophysiological alterations involved in rat hearts exposed to PM2.5 from diesel exhaust, termed as Diesel Particulate matter (DPM). In the present study, we explored the cardiovascular effect of DPM exposure on the recovery of heart from Ischemia reperfusion injury (IR) and explored the probable cause-effect relationship. Two groups of female Wistar rats were exposed to 0.5 mg/ml DPM for 1 h and 3 h durations daily for 21 days via a whole-body exposure system. At the end of 21st day, the animals were sacrificed and the heart was subjected to IR via Langendorff isolated rat heart perfusion system. 21 days of exposure altered cardiac electrophysiology and the ultra-structure of myocardium. Also, the same group of animals exhibited calcification in the vasculature. These changes were prominent in animals exposed to DPM for 3 h daily. Administration of DPM to H9C2 cells resulted in 15% and 36% cell death after 1hr and 3hrs of incubation, respectively. When the hearts were challenged to IR, both 1 h and 3 h exposed hearts exhibited a significant decline in IR recovery. At the sub-cellular level, DPM exposure reduced ATP levels, mitochondrial copy number, and increased oxidative stress after IR in both exposure groups. These changes were markedly seen in the interfibrillar mitochondrial fraction of the mitochondria. Hence, we conclude that exposure to PM2.5 from diesel exhaust alters electrophysiology and ultrastructure of heart and reduces the level of cellular mediators, thereby compromising the ability of heart to withstand IR injury.