Effects of inhaled prostacyclin as compared with inhaled nitric oxide in a canine model of pulmonary microembolism and oleic acid edema

Objective: Recently, it has been shown that the inhalation of nitric oxide (NO) and of prostacyclin (PGI(2)) elicits selective pulmonary vasodilation in a canine model of pulmonary hypertension induced by hypoxic pulmonary vasoconstriction. The present study was designed to investigate whether inhaled NO or PGI(2)-aerosol, respectively, is also effective in decreasing pulmonary artery pressure in a canine model of acute pulmonary microembolism and oleic acid edema. Design: Prospective, randomized, cross-over design. Setting: University animal research laboratory. Participants: Eight anesthetized, mechanically ventilated dogs (28 +/- 1 kg). Interventions: Acute pulmonary microembolization (PME) was induced using glass microbeads (mean diameter: 100 mu m) and 0.01 mL/kg of oleic acid. Subsequently, inhaled PGI(2) (concentration: 10 mu g/mL) or NO (50 ppm), respectively, was randomly administered for 15 minutes each and then withdrawn. Measurements and Main Results: Central hemodynamics (heart rate [HR], cardiac output [CO], stroke volume [SV], mean arterial pressure [MAP], systemic vascular resistance [SVR], mean pulmonary artery pressure [PAP], pulmonary vascular resistance [PVR]) and gas exchange (PaO2/FIO2 ratio, intrapulmonary shunt [Qs/Qt], alveolar-arterial oxygen difference, [AaDO(2)]) were assessed. Measurements were performed at control, after PME, and during administration of PGI(2) and NO, respectively. PME induced a significant increase (p < 0.001) of MAP (+9%), PAP (+68%), and PVR (+163%), whereas HR, CO, and SV remained unchanged and lung function deteriorated. Inhalation of NO slightly decreased PAP (-10%; p < 0.05) and PVR (-26%; p < 0.01) and improved AaDO(2) and PaO2/FIO2. In contrast, inhalation of PGI(2) had no consistent effect on pulmonary vascular tone or gas exchange. Conclusion: The data demonstrate that inhaled NO may elicit selective pulmonary vasodilation and improve gas exchange in a canine model of pulmonary microembolism and respiratory insufficiency. However, the degree of these effects was relatively small. The aerosolization of PGI(2) under conditions of positive-pressure ventilation did not exert a significant vasodilatory effect on pulmonary vessels and did not improve pulmonary gas exchange in this model. (C) 1995 by W.B. Saunders Company