Abstract

Nitric oxide (NO) is an important endothelium-dependent relaxing factor. In some pulmonary hypertensive states such as ARDS, the production of endogenous NO may be impaired. Nitric oxide inhalation selectively dilates the pulmonary circulation. Significant systemic vasodilation does not occur because NO is inactivated by rapidly binding to hemoglobin. In an injured lung with pulmonary hypertension, inhaled NO produces local vasodilation of well-ventilated lung units and may "steal" blood flow away form unventilated regions. This reduces intrapulmonary shunting and may improve systemic arterial oxygenation. Several observations require further study: 1. The hemodynamic and respiratory effects of NO inhalation vary, both among patients and within the same patient over the course of an illness. 2. Occasionally, sudden discontinuation of inhaled NO produces problematic pulmonary vasoconstriction. 3. NO inhalation may affect pulmonary structure and function and endogenous NO synthesis and transduction. Inhaled nitric oxide may have both beneficial and detrimental effects. 4. The safety and clinical efficacy of long-term NO administration remain unclear. Several randomized prospective clinical trials are beginning to address these issues. Potentially, inhaled NO may be a valuable therapy in a wide variety of patients with pulmonary hypertension and/or lung injury.