EFFECTS OF INHALED PROSTACYCLIN AS COMPARED WITH INHALED NITRIC-OXIDE ON RIGHT-VENTRICULAR PERFORMANCE IN HYPOXIC PULMONARY VASOCONSTRICTION

Objective: Recently, inhalation of prostacyclin (PGI(2)) has been shown to cause selective pulmonary vasodilation. However, the effects of inhaled PGI(2) on right ventricular (RV) performance are still unknown and therefore were compared with those of inhaled nitric oxide (NO). Design: Reported measurements design. Setting: Animal research laboratory. Animals: Six anesthetized, ventilated dogs (28 +/- 2 kg). Interventions: Pulmonary hypertension was induced by decreasing F1O2 to 0.09 - 0.11 ('hypoxic pulmonary vasoconstriction', HPV). Subsequently, a single dose of either NO (50 ppm) or PGI(2)-aerosol (0.9 +/- 0.3 ng/kg/min) was randomly added to the inspired gas. Measurements and Main Results: Measurements were performed before induction of HPV and 10 minutes after application and withdrawl of each drug. Central hemodynamics, global RV function, and local RV function (n = 5, sonomicrometry) were assessed. HPV resulted in an increase of pulmonary artery pressure (PAP), pulmonary vascular resistance (PVR), RV stroke work, right coronary artery flow, maximal rate of RV pressure increase (RV dP/dt(max)), and maximal velocity of shortening of contractile elements (V-max). In contrast, RV ejection fraction, RV end-diastolic volume, RV end-diastolic fiber length, and systolic fiber shortening were unchanged. Both PGI(2)-aerosol and NO attenuated the HPV-induced increase in PAP and PVR without affecting arterial pressure. NO, but not PGI(2), resulted in an increase of RV ejection fraction from 42 to 46% (P < 0.05). Right coronary flow dropped from 29 to ii mL/min during PGI(2) (p < 0.05). RV stroke work, RV dP/ dt(max), and V-max decreased subsequent to both NO and PGI(2), whereas local RV function was not affected. Conclusions: In pulmonary hypertension induced by HPV, PGI(2)-aerosol and inhaled NO reduced RV afterload and, hence, RV oxygen demand, with only minor changes of stroke volume and cardiac output, indicating an improvement of overall efficiency of RV contraction. RV ejection fraction increased on NO, but not with PGI(2). This might be explained by the fact that the reduction of pulmonary vascular resistance during PCI2 amounted to only 65% of the effect of NO. In summary, both inhaled NO and PGI(2)-aerosol showed beneficial effects on RV performance and may prove helpful in the treatment of acute pulmonary hypertension. Copyright (C) 1995 by W.B. Saunders Company