[Pulmonary hypertension: the role of nitric oxide in adults]

The human body releases endogenous nitric oxide (NO) from three main sources: neurons, inflammatory processes (induced NO) and endothelium. The chemical industry produces NO by reacting sulfur dioxide and nitric acid, or sodium nitrite and sulfuric acid, or by oxidation of ammonia. Inhaled NO acts on smooth muscle cells of the pulmonary endothelium, causing relaxation by stimulation of guanylate-cyclase. The short half life of NO and its immediate breakdown into hemodynamically inactive but toxic metabolites make this drug a selective pulmonary vasodilator that can decrease pulmonary arterial pressure, improving right ventricular ejection fraction while decreasing intrapulmonary shunt and improving oxygenation.NO has demonstrated its usefulness in treating right ventricular failure secondary to pulmonary hypertension after heart surgery, especially in the transplanted patient. Doses have usually ranged from 5 to 20 parts per million. However, great individual variability in response to NO has been reported. Between 30 and 40% of patients do not respond to treatment. NO is also used to assess the reversibility of chronic pulmonary hypertension in patients who are candidates for heart transplants. Other uses have been suggested, such as reversion of pulmonary vasoconstriction induced by protamine. Applications are limited by the toxicity of metabolites and by route of administration.