Relationship between basal nitric oxide and ventricular repolarization in an intact heart

Recent studies suggest that endogenous nitric oxide (NO) attenuates ischemia- or reperfusion-induced shortening in the action potential duration of ventricular myocytes. The effect of basal NO on ventricular repolarization in an intact heart remains unclear. The activation-recovery interval was measured from 32 epicardial electrocardiograms in six anesthetized, open-chest sheep. Intravenous administration of N^G-nitro-L-arginine, a NO synthase inhibitor, increased left ventricular systolic pressure from 101±7 mmHg to 118±10 mmHg (P=0.02), and left ventricular end diastolic pressure from 6.3±1.5 mmHg to 8.8±1.8 mmHg (P<0.01) without changing the heart rate (96±4 beats/min versus 94±3 beats/min, P=0.06). The average activation-recovery interval from the 32 ventricular sites remained unchanged in each animal after the administration of N^G-nitro-L-arginine (P>0.05). The pooled activation-recovery interval in the six animals before and 60 min after drug administration was 287±21 ms and 288±27 ms, respectively (P>0.05). It was concluded that basal NO is important in maintaining hemodynamics but has limited impact on ventricular repolarization.