[Inhaled nitric oxide in anesthesia and intensive care]

The role of endothelium in vascular relaxation is linked to the existence of endothelium derived relaxing factors (EDRF) known since 1980. In 1987, nitric oxide (NO) was identified as one of these factors. NO acts in many physiologic and pathophysiologic events. Atmospheric NO is a pollutant. Inhaled NO allows selective pulmonary vasodilation and is used to treat pulmonary artery hypertension (PAH). As inhaled NO is inactivated immediately in the blood by linking to haemoglobin, systemic vasodilation does not occur and right ventricular coronary perfusion pressure does not decrease. This is particularly important in the treatment of right ventricular failure due to PAH following cardiothoracic surgery. In patients with an acute respiratory distress syndrome (ARDS), inhaled NO improves the perfusion of adequately ventilated pulmonary territories. Very low concentrations of NO, such as two parts per million, decrease intrapulmonary venous admixture and may reverse hypoxaemia. However its long term benefits in ARDS must be assessed more accurately with multicentre controlled studies. Inhaled NO also improves refractory hypoxaemia in neonates. Its bronchodilatory effect, demonstrated experimentally, does not occur in acute obstructive bronchopulmonatory disease. The toxicity of NO, and overall of its oxidated derivative NO2 requires precise conditions of administration and close monitoring of inhaled fractions. In that case, the risk of NO toxicity seems very low when compared to its therapeutic benefits in selected patients.