INHALED NITRIC-OXIDE IN ANESTHESIA AND IN TENSIVE-CARE

The role of endothelium in vascular relaxation is linked to the existe nce of endothelium derived relaxing factors (EDRF) known since 1980, I n 1987, nitric oxide (NO) was identified as one of these factors. NO a cts in many physiologic and pathophysiologic events. Atmospheric NO is a pollutant. Inhaled NO allows selective pulmonary vasodilation and i s used to treat pulmonary artery hypertension (PAH), As inhaled NO is inactivated immediately in the blood by linking to haemoglobin, system ic vasodilation does not occur and right ventricular coronary perfusio n pressure does not decrease. This is particularly important in the tr eatment of right ventricular failure due to PAH following cardiothorac ic surgery, In patients with an acute respiratory distress syndrome (A RDS), inhaled NO improves the perfusion of adequately ventilated pulmo nary territories. Very low concentrations of NO, such as two parts per million, decrease intrapulmonary venous admixture and may reverse hyp oxaemia. However its long term benefits in ARDS must be assessed more accurately with multicentre controlled studies. inhaled NO also improv es refractory hypoxaemia in neonates, Its bronchodilatory effect, demo nstrated experimentally, does not occur in acute obstructive bronchopu lmonatory disease, The toxicity of NO, and overall of its oxidated der ivative NO2 requires precise conditions of administration and close mo nitoring of inhaled fractions. In that case, the risk of NO toxicity s eems very low when compared to its therapeutic benefits in selected pa tients.