• W M Zapol and W E Hurford.
• Department of Anesthesia, Massachusetts General Hospital, Boston, MA.
• New Horiz. 1993 Nov 1; 1 (4): 638-50.

AbstractIn 1987, nitric oxide was reported to be an endothelium-dependent relaxing factor. When inhaled as a gas at low levels, nitric oxide selectively dilates the pulmonary circulation. Significant systemic vasodilation does not occur because nitric oxide is inactivated by rapidly binding to hemoglobin. In an injured lung with pulmonary hypertension, inhaled nitric oxide produces local vasodilation of well-ventilated lung units and may "steal" blood flow away from unventilated regions. This reduces intrapulmonary shunting and may improve systemic arterial oxygenation. In patients with adult respiratory distress syndrome, inhaled nitric oxide reduces pulmonary hypertension and improves arterial oxygenation without reducing systemic arterial pressure. Tachyphylaxis to nitric oxide inhalation has not been observed. While additional chronic toxicology studies need to be performed, significant pulmonary toxicity has not been observed at low inhaled concentrations (< 80 parts per million by volume). Potentially, inhaled nitric oxide may be a valuable therapy in patients with adult respiratory distress syndrome.

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