Journal of Applied Physiology AJP: Cell Physiology
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J Appl Physiol 98: 739-747, 2005. First published October 29, 2004; doi:10.1152/japplphysiol.00556.2004
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HIGHLIGHTED TOPICS
Pulmonary Circulation and Hypoxia

Hypoxic pulmonary hypertension is prevented in rats with common bile duct ligation

Masatoshi Imamura,1 Bao Luo,2 Jennifer Limbird,1 Andrea Vitello,1 Masahiko Oka,1 D. Dunbar Ivy,3 Ivan F. McMurtry,1 Chrystelle V. Garat,1 Michael B. Fallon,2 and Ethan P. Carter1

1Cardiovascular-Pulmonary Research Laboratory, Department of Medicine, University of Colorado Health Sciences Center, Denver; 2Department of Internal Medicine and Liver Center, University of Alabama at Birmingham, Birmingham, Alabama; and 3Pediatric Heart Lung Center and Section of Pediatric Cardiology, Department of Pediatrics, University of Colorado Health Sciences Center and The Children's Hospital, Denver, Colorado

Submitted 27 May 2004 ; accepted in final form 22 October 2004

Biliary cirrhosis in the rat triggers intrapulmonary vasodilatation and gas-exchange abnormalities that characterize the hepatopulmonary syndrome. This vasodilatation correlates with increased levels of pulmonary microcirculatory endothelial NO synthase (eNOS) and hepatic and plasma endothelin-1 (ET-1). Importantly, during cirrhosis, the pulmonary vascular responses to acute hypoxia are blunted. The purpose of this work was to examine the pulmonary vascular responses and adaptations to the combination of liver cirrhosis and chronic hypoxia (CH). In addition to hemodynamic measurements, we investigated whether pulmonary expression changes of eNOS, ET-1 and its receptors (endothelin A and B), or heme oxygenase 1 in experimental cirrhosis affect the development of hypoxic pulmonary hypertension. We induced cirrhosis in male Sprague-Dawley rats using common bile duct ligation (CBDL) and exposed them to CH (inspired PO2 {approx} 76 Torr) or maintained them in Denver (Den, inspired PO2 {approx} 122 Torr) for 3 wk. Our data show 1) CBDL-CH rats had a persistent blunted hypoxic pulmonary vasoconstriction similar to CBDL-Den; 2) the development of hypoxic pulmonary hypertension was completely prevented in the CBDL-CH rats, as indicated by normal pulmonary arterial pressure and lack of right ventricular hypertrophy and pulmonary arteriole remodeling; and 3) selective increases in expression of ET-1, pulmonary endothelin B receptor, eNOS, and heme oxygenase 1 are potential mechanisms of protection against hypoxic pulmonary hypertension in the CBDL-CH rats. These data demonstrate that unique and undefined hepatic-pulmonary interactions occur during liver cirrhosis and chronic hypoxia. Understanding these interactions may provide important information for the prevention and treatment of pulmonary hypertension.

hepatopulmonary syndrome; chronic hypoxia; hypoxic pulmonary vasoconstriction; right ventricular hypertrophy; polycythemia; nitric oxide


Address for reprint requests and other correspondence: E. P. Carter, Campus Box B-133, 4200 East 9th Ave., Denver, CO 80262 (E-mail: ethan.carter{at}uchsc.edu)




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