Inhaled prostacyclin (PGI₂) versus inhaled nitric oxide in adult respiratory distress syndrome

Inhalation of nitric oxide (NO) and prostacyclin (PGI₂) may induce selective pulmonary vasodilation and-by improving ventilation-perfusion ratio in ventilated areas of the lung-increase Pa(O₂) in patients with acute lung injury. To assess the therapeutic efficacy of both compounds, dose-response curves were established in patients with adult respiratory distress syndrome (ARDS). Patients received both PGI₂ (doses of 1, 10, and 25 ng/kg/min) and NO (concentrations of 1, 4, and 8 ppm). Cardiorespiratory parameters were assessed at control, at each d rug concentration, and after withdrawal of NO and PGI₂. PGI₂ resulted in a significant, dose-dependent and selective reduction of pulmonary artery pressure (PAP) from 35.1 ± 6.3 mm Hg at control to 33.1 ± 4.8 (1 ng/kg/min), 31.3 ± 4.8 mm Hg (10 ng/kg/min) and 29.6 ± 4.5 mm Hg (25 ng/kg/min), respectively. Inhaled NO reduced PAP from 34.5 ± 5.6 to 32.1 ± 5.9 mm Hg at 4 ppm, and to 31.8 ± 6.1 mm Hg at 8 ppm, respectively, with no effect at 1 ppm. Pa(O₂)/Fl(O₂) ratio increased from 105 ± 37 to 125 ± 56 mm Hg (range of increase: 0 to 57 mm Hg) at PGI₂ 10 ng/kg/min and to 131 ± 63 mm Hg (range: -5 to 89 mm Hg) at 25 ng/kg/min with no effect at 1 ng/kg/min. NO improved Pa(O₂) (e.g., from 116 ± 47 to 167 ± 86 mm Hg at 8 ppm) and reduced intrapulmonary shunt at all doses tested. We conclude that both inhaled PGI₂ and NO may induce selective pulmonary vasodilation and increase Pa(O₂) in severe ARDS.