Introduction: Ambient particulate matter (PM) can increase cardiac arrhythmias via oxidative stress. This study was performed to reveal that the heat shock protein, α B-crystallin, could prevent the arrhythmogenic effect of PM. Methods: Using optical mapping, arrhythmic mechanism were evaluated in Langendorff-perfused Adult Sprague-Dawley rat heart after infusion of diesel exhaust product (DEP) and αB-crystallin. Results: In neonatal rat cardiomyocytes, DEP provoked cell death and ROS generation in dose dependant manner. In Langendorff-perfused rat hearts, DEP infusion of 12.5 mg/L (n=12) prolonged action potential duration (APD90) at only the base of left ventricle (LV) from 101± 14 ms to 152± 22 ms (p=0.001) increasing apicobasal APD differences from 4± 8 ms to 54± 25 ms (p=0.003). Pretreatment of aB-crystallin (1 mg/kg, n=9) with a delivery system (TAT-protein transduction domain) prevented the DEP-induced APD prolongation (106± 10 ms, p=0.83) and apicobasal APD differences (1.5± 15.5 ms, p=0.83). Compared with DEP alone, pretreatment of αB-crystallin decreased triggered activity (67% vs. 11%, p=0.02) and apicobasal reentry (82% vs. 0%, p=0.001). The ventricular tachyarrhythmia (VT) was observed in 9 (75%) and 4 (44%) hearts after DEP alone and pretreatment of αB-crystallin (p=0.04), respectively. Conclusions: Heat shock protein, αB-crystallin, can prevent arrhythmogenic effect of PM by suppressing apicobasal repolarization gradient and triggered activity.
All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine