Exp Clin Cardiol. 2003;8(1):10-2.
Experimental and clinical cardiology
Lexin Wang
PMID: 19644580 PMCID: PMC2716192
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.
Keywords: Activation-recovery interval; Cardiac electrophysiology; Nitric oxide; Ventricular repolarization
