Nitric oxide (NO), which is normally released by endothelial cells including those of pulmonary bed, serves to modulate vascular tone by relaxing the subjacent smooth muscle cells. Recently, administration of NO by inhalation was found to produce selective vasodilatation of the pulmonary circulation ( Higgenbottamefa/.., 1988). Once in the alveoli, inhaled NO diffuses to the smooth muscle cells of the pulmonary vessels and to the blood perfusing the lung where it is inactivated. Several mechanisms of inactivation have been suggested, including binding of hemoglobin in red cells or other blood proteins by NO.

Low fractions of inhaled NO (18-36 ppm) have been reported to lower pulmonary arterial pressure and improve arterial oxygenation in adult respiratory distress syndrome patients in the intensive care unit (ICU) ( Rossaintetal 1993). Several authors have suggested that inhaled NO is distributed predominantly to well-ventilated alveoli and is not delivered to collapsed or fluid-filled areas of the lung. Consequently, local vasodilation of well-ventilated lung regions induces a

gradient for regional conductance, leading to diversion of pulmonary arterial blood flow towards well-ventilated alveoli and improving ventilation-perfusion ( V/Q) mismatch and arterial oxygenation. We have recently shown that such a gradient can be enhanced by using almitrine bismesylate, a vasoconstrictive agent that acts preferentially on the vessels of poorly ventilated lung regions, reinforcing hypoxic vasoconstriction ( Payen.efa/ 1993), P§y§0„„§La/., (1996).

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