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

B. Zwissler, G. Kemming, O. Habler, M. Kleen, Matthias Merkel, M. Haller, J. Briegel, M. Welte, K. Peter

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226 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)1671-1677
Number of pages7
JournalAmerican Journal of Respiratory and Critical Care Medicine
Issue number6
Publication statusPublished - 1996
Externally publishedYes


ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

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