Inhaled nitric oxide has been reported to act as a specific pulmonary vasodilator. We used the newborn piglet to create acute hypoxic pulmonary hypertension and examined the effect of inhaled nitric oxide in this model. Six newborn piglets were instrumented in order to measure cardiac index, pulmonary arterial pressure, and systemic arterial pressure. Pulmonary hypertension was induced by reducing the fraction of inspired oxygen to 0.12 to 0.14. With hypoxia (arterial oxygen saturation between 35 and 45%), pulmonary arterial pressure increased by 48% (p < 0.01), pulmonary vascular resistance increased by 74% (p < 0.01), and both systemic arterial pressure and systemic vascular resistance decreased by 38 and 31%, respectively (p < 0.01). The animals were then giving varying concentrations of inhaled nitric oxide between 5 and 80 parts per million in random order. All concentrations of nitric oxide were associated with a rapid decrease in pulmonary arterial pressure and pulmonary vascular resistance (p < 0.001). Cardiac index increased (p < 0.001) and systemic vascular resistance significantly decreased (p = 0.01) with all doses of inhaled nitric oxide. The ratio of pulmonary to systemic vascular resistance decreased with all levels of inhaled nitric oxide (p < 0.001). For all of the above observations there was no significant difference noted between the varying doses of nitric oxide. The time course of the pulmonary arterial pressure response to nitric oxide was approximately twice as fast as that seen with the inhalation of 100% oxygen (10, 50, 90% responses of 4.1, 8.8, 88.6 versus 6.7, 51.9, 197 s, respectively; p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)