INHALED PROSTACYCLIN (PGI(2)) VERSUS INHALED NITRIC-OXIDE IN ADULT-RESPIRATORY-DISTRESS-SYNDROME

Inhalation of nitric oxide (NO) and prostacyclin (PCl2) may induce sel ective pulmonary vasodilation and-by improving ventilation-perfusion r atio in ventilated areas of the lung-increase Pa-O2 in patients with a cute lung injury. To assess the therapeutic efficacy of both compounds , dose-response curves were established in patients with adult respira tory distress syndrome (ARDS). Patients received both PGl(2) (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 drug co ncentration, and after withdrawal of NO and PGl(2). PCl2 resulted in a significant, dose-dependent and selective reduction of pulmonary arte ry 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 fr om 105 +/- 37 to 125 +/- 56 mm Hg (range of increase: 0 to 57 mm Hg) a t PGl(2) 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 intrapulmo nary shunt at all doses tested. We conclude that both inhaled PGl(2) a nd NO may induce selective pulmonary vasodilation and increase Pa-O2 i n severe ARDS.