Azoto monoksido poveikio ypatumai ir panaudojimas ūmaus kvėpavimo nepakankamumo metu

Abstract

Nitric oxide is an important endothelium-relaxing factor. NO is a selective pulmonary vasodilator in adult and pediatric patients and may be a useful therapeutic agent in the treatment of patients with severe pulmonary hypertension from a variety of causes. When inhaled as a gas at low levels, NO selectively dilates the pulmonary circulation. Significant systemic vasodilation does not occur because NO is inactivated by rapidly binding to hemoglobin. Inhaled NO is also effective in treating hypoxemia as it improves ventilation to perfusion matching and decreases pulmonary shunt. In an injured ARDS lung with pulmonary hypertension, inhaled NO produces local vasodilation of well-ventilated lung units and may "steal" blood flow from unventilated regions. This reduces intrapulmonary schunting and may improve systemic arterial oxygenation. Potencially, inhaled NO may be a valuable therapy in ARDS patients with acute lung injury and pulmonary hypertension. Large clinical trials will determine if inhaled NO decreases mortality or improves ventilator weaning. The most important questions regarding inhaled NO therapy concern its potential toxicity.