Introduction: Recent evidences suggest that ambient particulate matter (PM) can increase cardiac arrhythmias via oxidative stress. AlphaB-crystallins (慣B-crystallin), members of the small heat shock protein 20 family, can be induced by heat shock and can prevent the ischemic injury. This study evaluated whether 慣B-crystallin could prevent the arrhythmogenic effect of PM.

Methods: In vivo experiment was performed by tracheal exposure of DEP of 100mg/L, 200mg/L, 400mg/L and/or 慣B-crystallin in Adult Sprague-Dawley rats (n=23). Using optical mapping, arrhythmic events and mechanism were evaluated in Langendorff-perfused rat heart (n=21). 慣B-crystallin was delivered into cardiac cells using TAT-protein transduction domain.

Results: The tracheal exposure of DEP increased premature ventricular contractions and prolonged QT interval, dose dependently. However, pretreatment of 慣B-crystallin (5mg/kg) prevented these effects. In Langendorff-perfused rat hearts, DEP infusion of 12.5 mg/L for 20 minutes (n=12) prolonged action potential duration (APD90) at only the base of left ventricle from 101짹14 ms to 152짹22 ms (p=0.001) increasing apicobasal APD differences from 4짹8 ms to 54 짹 25 ms (p=0.003). Pretreatment of 慣B-crystallin (1 mg/kg, n=9) for 20 min prevented the DEP-induced APD prolongation (106 짹 10 ms, p=0.83) and apicobasal APD differences (1.5 짹 15.5 ms, p=0.83). The pacing cycle length for inducing spatially discordant alternans also decreased after 慣B-crystallin pretreatment (86.7 짹 7.6 ms) than DEP alone (119.3 짹 17.4 ms, p=0.02). Compared with DEP alone, pretreatment of 慣B-crystallin decreased triggered activity from 75% to 22% (p=0.02) and ventricular tachyarrhythmia from 75% to 11% (p=0.005).

Conclusions: Ambient PM increased apicobasal repolarization gradient, triggered activity and ventricular tachyarrhythmia. Heat shock protein, 慣B-crystallin, could prevent arrhythmogenic effects of PM by suppressing apicobasal repolarization gradient and triggered activity.