INHALED NITRIC-OXIDE SELECTIVELY DECREASES PULMONARY-ARTERY PRESSURE AND PULMONARY VASCULAR-RESISTANCE FOLLOWING ACUTE MASSIVE PULMONARY MICROEMBOLISM IN PIGLETS

Acute massive pulmonary embolism increases pulmonary artery pressure ( PAP) and pulmonary vascular resistance (PVR), which may lead to early right ventricular failure and subsequent cardiocirculatory deteriorati on. Inhaled nitric oxide (NO) selectively dilates pulmonary vessels in vivo. Thus, inhaled NO may be useful in preventing cardiocirculatory deterioration following pulmonary embolism. We investigated the effect s of inhaled NO in the acute phase of massive pulmonary microembolism in 10 anesthetized and mechanically ventilated piglets (body weight, 1 8+/-2 kg), Microspheres of 300-mu m diameter were injected IV in an am ount sufficient to initially increase mean PAP to 45 mm Hg. Forty-five minutes after pulmonary embolization, the pretreatment control values were recorded. Thereafter, the piglets inhaled 40 ppm NO, and subsequ ently 80 ppm NO. When 40 ppm NO was inhaled, there was a significant d ecrease in systolic PAP (-10.3%; 44.5+/-2.2 to 39.9+/-2.4 mm Hg; p<0.0 5) and mean PAP (-9.4%; 32.9+/-1.3 to 29.8+/-1.3 mm Hg; p<0.05). PVR w as changed by -13.6% (p=0.07). Administration of 80 ppm NO resulted in a significant decrease in systolic PAP (-12.6%; to 38.9 +/- 1.9 mm Hg ; p<0.05), mean PAP (-11.9%; to 29.0+/-1.4 mm Hg; p<0.05), and PVR (-1 9.4%; p<0.05) compared with pretreatment values. Discontinuation of NO inhalation was associated with an immediate return to pretreatment va lues. Systemic hemodynamics and the arterial and mixed venous oxygen c oncentrations remained unchanged. We conclude that inhaled NO followin g acute massive pulmonary microembolism selectively decreases PAP and PVR without influencing systemic hemodynamics in piglets.