Prolonged Ventricular Action Potential Duration Due to Nitric Oxide Release

Background evious study has demonstrated that increased intracoronary perfusion leads to a flow-dependent inversion of T waves on body surface ECG. However, whether increased coronary flow influences ventricular action potential duration measured directly from myocardium is unknown. s pentobarbital-anesthetized sheep, fresh arterial blood was injected into the left circumflex coronary (LCX) artery at a rate of 6 and 10 mL/min, respectively, in the presence of normal coronary flow. Activation−recovery interval (ARI), an estimate of ventricular action potential duration, was measured from epicardial ECGs acquired from the LCX territory. s tracoronary injection prolonged ARI by an average of 21 ± 9 and 33 ± 14 msec, respectively. After pre-treatment with nitro-l-arginine, a nitric oxide synthase inhibitor, intracoronary injection at the rate of 6 and 10 mL/min lead to an ARI increase of 3 ± 2 msec (p >0.05) and 11 ± 6 msec (p <0.05) respectively. sions rease in coronary flow prolongs ventricular action potential duration in the intact sheep heart. Nitric oxide mediates the injection-induced increase in action potential duration.