L-ARGININE INCREASES EXERCISE-INDUCED VASODILATION OF THE FOREARM IN PATIENTS WITH HEART-FAILURE

To determine whether L-arginine, a precursor of nitric oxide, can impr ove exercise-induced vasodilation of the forearm in patients with hear t failure, we measured forearm blood flow in 9 patients with heart fai lure and in 7 age-matched control subjects before and after intra-arte rial infusion of L-arginine. Resting forearm blood flow was significan tly lower in patients with heart failure than in control subjects (2.3 4 +/- 0.85 (SD) vs 4.76 +/- 0.77 ml/min per 100 ml, p < 0.001). Endoth elium-dependent vasodilation induced by acetylcholine was attenuated i n patients with heart failure (p < 0.05). Exercise-induced vasodilatio n after handgrip exercise was significantly lower in patients with hea rt failure (p<0.05). Intra-arterial infusion of L-arginine did not cha nge basal forearm blood now but significantly augmented acetylcholine- induced vasodilation in both patients with heart failure and control s ubjects (p<0.05). Although L-arginine did not affect maximum forearm b lood flow after handgrip exercise in control subjects (before, 26.2 +/ - 13.5; after, 25.7 +/- 14.3; p = NS), it was increased in patients wi th heart failure (from 15.2 +/- 4.9 to 24.7 +/- 14.6, p < 0.01). The f inding that L-arginine increased both acetylcholine- and exercise-indu ced vasodilation in patients with heart failure suggests that endothel ial dysfunction might play an important role in impaired exercise-indu ced vasodilation in patients with heart failure.