摘要
N-n-butyl haloperidol iodide (F2), a novel quaternary ammonium salt derivative of haloperidol, was reported to antagonize myocardial ischemia/reperfusion injuries. To investigate its mechanisms, we characterized the effects of F2 on Na+/Ca2+ exchanger currents (INCX) and the L-type Ca2+ channel current (ICa,L) of cardiomyocytes during either hypoxia/reoxygenation or exposure to H2O2. Using whole-cell patch-clamp techniques, the INCX and ICa,L were recorded from isolated rat ventricular myocytes. Exposure of cardiomyocytes to hypoxia/reoxygenation or H2O2 enhanced the amplitude of the inward and outward of INCX and ICa,L. F2 especially inhibited the outward current of Na+/Ca2+ exchanger, as well as the ICa,L, in a concentration-dependent manner. F2 inhibits cardiomyocyte INCX and ICa,L after exposure to hypoxia/reoxygenation or H2O2 to antagonize myocardial ischemia/reperfusion injury by inhibiting Ca2+ overload.