Preconditioning with PEP-1-SOD1 fusion protein attenuates ischemia/reperfusion-induced ventricular arrhythmia in isolated rat hearts.

PEP 1-Cu/Zn superoxide dismutase (PEP-1-SOD1) fusion protein preconditioning has been reported to protect the myocardium from ischemia/reperfusion (I/R)-induced injury by decreasing the infarct size, reducing levels of cardiomyocyte apoptosis and reducing the release of myocardial-specific biomarkers. The aim of the present study was to examine the effects of PEP-1-SOD1 pretreatment on I/R-induced ventricular arrhythmias in Langendorff-perfused rat hearts. The isolated rat hearts were pretreated with PEP-1-SOD1 prior to I/R, and the I/R-induced hemodynamic parameters, infarct size and ventricular arrhythmias were then assessed. Compared with the unprotected hearts, PEP-1-SOD1 preconditioning significantly improved the hemodynamic parameters, decreased the cardiac lactate dehydrogenase and creatine kinase-MB (CK-MB) levels, reduced the infarct size and attenuated the ventricular arrhythmia. Further investigation showed that PEP-1-SOD1 preconditioning reduced both the incidence and duration of ventricular tachycardia/ventricular fibrillation. In addition, the intracellular reactive oxygen species (ROS) levels were decreased. The results of the present study suggest that PEP-1-SOD1 preconditioning can protect the heart against I/R injury and attenuate I/R-induced arrhythmia by downregulating the generation of ROS.