PGI2 AEROSOL VERSUS NITRIC-OXIDE FOR SELECTIVE PULMONARY VASODILATIONIN HYPOXIC PULMONARY VASOCONSTRICTION

Intravenous prostacyclin (PGI2) is a potent pulmonary vasodilator in p ulmonary hypertension. However, dose-dependent systemic vasodilation, an increase in intrapulmonary shunt and hypoxemia limit its clinical a pplication. Recently, inhaled nitric oxide (NO) has been reported to e licit selective pulmonary vasodilation, but its clinical use is restri cted by its potential toxicity; furthermore, the feasibility of NO app lication in clinical practice seems difficult. Therefore, we investiga ted the effects of PGI2 aerosol on pulmonary and systemic circulation and compared the hemodynamic effects to those of inhaled NO. In 6 dogs , ventilation with a hypoxic gas mixture (FiO2 0.09-0.11) increased pu lmonary vascular resistance (PVR) by 196% (HPV). Aerosolization of a P GI2 solution at a concentration of 430 ng/ml reduced hypoxia-induced i ncrease of pulmonary artery pressure by 48% and PVR by 52% within 6-10 min without systemic vasodilation. The administered dose of PGI2 was 0.87 +/- 0.26 ng/kg/min. In 2 dogs, doubling the PGI2 concentration (8 60 ng/ml) did not enhance the vasodilatory effect. After termination o f PGI2 inhalation, HPV was restored within 10-15 min. Inhaled NO (50 p pm) decreased the HPV-induced increase in PAP by 76% and in PVR by 73% within 5-10 min. Clinically relevant systemic vasodilation was not ob served. It is concluded that inhalation of aerosolized PGI2 leads to s elective pulmonary vasodilation in hypoxia-induced pulmonary hypertens ion. Aerosolized PGI2 at a concentration of 430 ng/ml was less potent than NO (50 ppm). However, due to the lack of known toxicity and its u ncomplicated mode of application, inhaled PGI2 may be one alternative to inhaled NO in the treatment of acute pulmonary hypertension.