toward lung regions with better ventilation and a higher intraalveolar partial pressure of oxygen. Inhaled NO enhances this mechanism by increasing blood flow to well-ventilated lung areas that, in some diseases, have an elevated vasomotor tone. This vasodilatory effect of inhaled NO is in marked contrast to intravenously administered vasodilators. Such intravenous agents produce diffuse dilation of the pulmonary vasculature, including areas of nonventilated lung, thereby increasing intrapulmonary shunting and reducing the PaO2 (Figure 2). The beneficial effects of inhaled NO to reduce intrapulmonary shunting and oxygenation have been demonstrated in patients with acute respiratory distress syndrome. 13, 14