Abstract
PURPOSE: The aim of the study was to investigate the effect of sertraline on the rat heart during ischemia and reperfusion and to determine its effect on NO production. MATERIALS AND METHODS: The study was performed on isolated rat hearts. Hearts from three groups were perfused with sertraline at three different concentrations and subjected to global ischemia and reperfusion. Hearts from the other three groups were perfused with the same concentrations of sertraline but without the ischemia/reperfusion process. Two control groups were perfused with the Krebs-Henseleit solution only with and without ischemia/reperfusion process. Coronary flow (CF), heart rate (HR), left ventricular developed pressure (LVDP) and maximum rate of rise of left ventricular pressure (dP/dt max) were measured. Perfusate effluent was collected to determine creatine phosphokinase (CPK) and nitrate plus nitrite (NOx) levels. RESULTS: In non-ischemic groups, sertraline at the concentration of 10 μmol/L exerts a strong vasodilatory effect on CF, and after a short positive inotropic effect, it exerts a strong inotropic and chronotropic negative effect on isolated rat hearts and causes a direct damage to cardiomyocytes. At the concentration of 1 μmol/L, sertraline exerts an increasing negative inotropic effect. There were no hemodynamic differences between any of groups of hearts subjected to reperfusion. Sertraline had no effect on the nitric oxide concentration in coronary effluent neither in rat hearts subjected to ischemia/reperfusion nor in non-ischemic conditions. CONCLUSION: Sertraline at dose 10 μmol/L exerts a strong vasodilatory effect on coronary flow, and after a short positive inotropic effect, it exerts a strong negative effect on isolated rat hearts, causing a direct damage to cardiomyocytes. Sertraline had no effect on the nitric oxide concentration in coronary effluent.