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Articles in PresS, published online ahead of print March 29, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00385.2001
Submitted on September 28, 2001
Accepted on March 26, 2002
1 Cardiovascular-Pulmonary Research Laboratory, University of Colorado Health Sciences Center, Denver, Colorado, USA; Physiology & Biophysics, University of Colorado Health Sciences Center, Denver, Colorado, USA
2 Cardiovascular-Pulmonary Research Laboratory, University of Colorado Health Sciences Center, Denver, Colorado, USA
* To whom correspondence should be addressed. E-mail: Ethan.Carter{at}uchsc.edu.
During hepatopulmonary syndrome caused by liver cirrhosis, pulmonary eNOS expression and NO production are increased. Increased NO contributes to the blunted hypoxic pressor response (HPR) during cirrhosis and may induce heme oxygenase-1 (HO-1) expression and carbon monoxide (CO) production exacerbating the blunted HPR. We hypothesized that NO regulates the expression of HO-1 during cirrhosis, contributing to hepatopulmonary syndrome. Cirrhosis was induced in rats by common bile duct ligation (CBDL). Rats were studied 2- and 5-wk following CBDL or sham surgery. Lung HO-1 expression was elevated 5 wk following CBDL. Liver HO-1 was increased at 2 wk and remained elevated at 5 wk. In catheterized rats, the blunted HPR was partially restored by HO inhibition. Rats treated with the NOS inhibitor L-NAME for the entire 2- or 5-wk duration had normalized HO-1 expression and HPR. These data provide in vivo evidence for the NO-mediated upregulation of HO-1 expression and support the concept that hepatopulmonary syndrome is multifactorial involving not only NO, but also HO-1 and CO.
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