ENHANCED BASAL NITRIC-OXIDE PRODUCTION IN HEART-FAILURE - ANOTHER FAILED COUNTER-REGULATORY VASODILATOR MECHANISM

Endothelial dysfunction in heart failure could impair nitric oxide pro duction and lead to increased vascular resistance. If endogenous produ ction of nitric oxide is reduced, N-G-monomethyl-L-arginine (L-NMMA), an inhibitor of such production, should have a diminished vasoconstric tor effect. We administered L-NMMA to 12 patients being investigated f or heart failure. L-NMMA increased median pulmonary and systemic vascu lar resistances by 61 (range - 3 to 240) and 430 (63 to 1609)dynes s c m(-5), respectively (p<0.03 and p<0.005). Arterial pressures also incr eased. Median cardiac output fell by 0.6 (0 to -2.3) L per min (p<0.00 5). These data suggest that vascular nitric oxide may be another examp le of a failed counter-regulatory vasodilator system in heart failure.