Inhaled nitric oxide: its effects on pulmonary circulation and airway smooth muscle cells.

Abstract

Nitric oxide (NO), an endothelium-derived relaxing factor synthesized from L-arginine by the enzyme NO synthase, has been identified as an important, short-acting, endogenous vasodilator. In patients with pulmonary hypertension, inhaling a low dose of NO as a gaseous vasodilator has been shown to induce selective vasodilation in ventilated lung areas. It achieves this without the disadvantages attributed to systemically infused vasodilators e.g. systemic vasodilation and an increase in pulmonary right-to-left shunt with a consecutive fall in PaO2. Thus, inhaled NO reduces pulmonary hypertension in the severe adult respiratory distress syndrome and in persistent pulmonary hypertension of the newborn, and improves arterial oxygenation by redistributing pulmonary blood flow away from the shunt and towards areas with almost normal ventilation/perfusion ratios. The bronchodilatory effect of NO may be an alternative therapy for treating asthma and bronchospasm.