L-ARGININE IMPROVES ENDOTHELIUM-DEPENDENT RELAXATION OF CONDUCTANCE AND RESISTANCE CORONARY-ARTERIES IN CORONARY-ARTERY DISEASE

To assess the ability of L-arginine to improve endothelium-dependent vasodilation in atheromatous coronary arteries, we determined whether intracoronary infusion Of L-arginine could improve coronary vascular reactivity to acetylcholine (ACh) examining both conductance and resistance vessels. Coronary blood flow velocity was assessed by positioning a 3 Fr Doppler catheter into the proximal coronary artery segment (six left anterior descending and one circumflex coronary artery). Computed quantitative angiography allowed the measurement of distal diameters. After baseline measurements, ACh was infused at incremental infusion rates through the Doppler lumen catheter (3 min period each) to obtain the estimated concentrations of 5 x 10(-7), 10(-6), and 5 x 10(-6) M. After returning to baseline, L-arginine was infused at the rate of 25 mg/min (10(-3) M) through the Doppler lumen catheter. Infusion of ACh was then repeated according to the same protocol than in the absence Of L-arginine. The heart rate and mean arterial blood pressure did not change at any step of the protocol. Infusion of ACh induced dose-dependent vasoconstriction of coronary distal segments with a reduction in coronary distal segments by 39 +/- 15% at 5 x 10(-6) M (p < 0.01). During infusion of L-arginine, the coronary diameter was reduced by only 16 +/- 10% (p < 0.05) at the highest ACh dose. The coronary blood flow velocity increased by 100 +/- 15% at 5 x 10(-7) M ACh (p < 0.05) but only to 16 +/- 15% at 5 x 10(-6) M ACh (NS). During L-arginine infusion, ACh induced an increase in coronary blood flow velocity at the three serial ACh doses. At the highest ACh dose, the coronary blood flow velocity was increased by 65 +/- 11% (p < 0.01 vs. without L-arginine). The results show than in patients with coronary artery disease. infusion of L-arginine alleviates the vasoconstrictor action of ACh, suggesting improvement of endothelium-dependent relaxation in coronary arteries by L-arginine both on conductance and resistance vessels.