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Inhaled nitric oxide reduces pulmonary artery pressures in portopulmonary hypertension
Author(s) -
Findlay James Y.,
Harrison Barry A.,
Plevak David J.,
Krowka Michael J.
Publication year - 1999
Publication title -
liver transplantation and surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.814
H-Index - 150
eISSN - 1527-6473
pISSN - 1074-3022
DOI - 10.1002/lt.500050515
Subject(s) - portopulmonary hypertension , medicine , pulmonary artery , inhalation , pulmonary hypertension , vascular resistance , cardiology , liver transplantation , nitric oxide , cardiac output , hemodynamics , transplantation , anesthesia
Abstract Pulmonary artery hypertension in association with liver failure (portopulmonary hypertension [PPHTN]) is a significant barrier to liver transplantation because patients with this condition have a very high mortality when transplantation is undertaken. Inhaled nitric oxide (NO), a potent pulmonary vasodilator, reduces pulmonary artery pressure (PAP) in some patients with primary pulmonary hypertension, but its effect in patients with PPHTN is controversial. We investigated the hemodynamic effects of inhaled NO in 6 patients with PPHTN. Five of 6 patients responded to NO inhalation with decreases in PAP and pulmonary vascular resistance of greater than 10%; these decreases were statistically significant at NO concentrations of 10 and 30 ppm. Cardiac output did not significantly change. We conclude that inhalation of NO reduces PAPs in some patients with PPHTN.