NITRIC-OXIDE REVERSES ACUTE HYPOXIC PULMONARY-HYPERTENSION IN THE NEWBORN PIGLET

Inhaled nitric oxide has been reported to act as a specific pulmonary vasodilator. We used the newborn piglet to create acute hypoxic pulmon ary hypertension and examined the effect of inhaled nitric oxide in th is model. Six newborn piglets were instrumented in order to measure ca rdiac index, pulmonary arterial pressure, and systemic arterial pressu re. Pulmonary hypertension was induced by reducing the fraction of ins pired oxygen to 0.12 to 0.14. With hypoxis (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), an d both systemic arterial pressure and systemic vascular resistance dec reased by 38 and 31%, respectively (p < 0.01). The animals were then g iving 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 a nd 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 pulmona ry to systemic vascular resistance decreased with all levels of inhale d nitric oxide (p < 0.001). For all of the above observations there wa s 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 inh alation 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). Inhaled nitric oxide at le vels of 5 parts per million or greater reverses hypoxia-induced pulmon ary vasoconstriction in the newborn piglet model.