Small doses of carbon monoxide from the CORM-2 donor drug reduce ischemia-reperfusion damage to the heart

Abstract

The study investigates the cardioprotective effects of small doses of carbon monoxide released from the donor drug CORM-2 during ischemia-reperfusion injury in isolated mouse hearts. Administration of CORM-2 stabilized coronary flow, reduced Ca²⁺ deposition, and decreased creatinine and aspartate aminotransferase release, indicating improved mitochondrial function and reduced cytoplasmic membrane damage. Electrophysiological analysis revealed modulation of ventricular depolarization, particularly changes in the amplitude of the R wave. These findings suggest that CORM-2 exerts protective effects against ischemia-reperfusion injury, likely through interactions with calcium channels and energy metabolism, supporting its potential as a therapeutic agent in myocardial ischemia.