Short-term Pulmonary Vasodilation With l-Arginine in Pulmonary Hypertension

Background Endothelial dysfunction may contribute to the pathogenesis of pulmonary hypertension through impaired production of the endothelium-derived vasodilator nitric oxide (NO). l-Arginine, the substrate for NO synthase (NOS), has a vasodilatory effect in systemic vascular beds and can correct abnormal endothelium-dependent vasodilation. It has been suggested that these two effects of l-arginine are mediated through NOS metabolism and enhanced NO production. Therefore, we assessed the short-term pulmonary hemodynamic effects of exogenous l-arginine in patients with pulmonary hypertension of various origins. Methods and Results During continuous hemodynamic monitoring, 10 subjects with pulmonary hypertension (mean pulmonary artery pressure [PAP], 54±5 mm Hg [mean±SEM]) received a 30-minute control infusion of hypertonic saline followed by a 30-minute infusion of 500 mg/kg of l-arginine. The hemodynamic effects of l-arginine were compared with those of prostacyclin titrated to maximally tolerated doses....