Influence of phenobarbital on changes in Na(+) handling, hemodynamics and liver function due to partial portal vein ligation in rats.
This study examined the influence of phenobarbital, an inducer of hepatic enzymes, on Na(+) handling, hemodynamics and liver function (measured by the rate constant of elimination of aminopyrine in the aminopyrine breath test) after partial portal vein ligation. Rats were randomized to drink either phenobarbital + water or water only for 10 days and then underwent either sham operation or partial portal vein ligation. The aminopyrine rate constant of elimination and Na(+) balance were measured daily before and after surgery; after surgery, hemodynamic measurements were obtained daily in a subset of rats. Phenobarbital raised the baseline aminopyrine rate constant of elimination. Partial portal vein ligation, but not sham operation, caused equivalent reductions in the aminopyrine rate constant of elimination in phenobarbital- and water-treated groups, such that the aminopyrine rate constant of elimination remained higher in the former. Na(+) balance increased significantly in partial portal vein ligation + water, but not sham + water rats on day 1 and then decreased on days 2 and 3. In contrast, neither sham + phenobarbital nor partial portal vein ligation + phenobarbital rats had a significant increase in Na(+) balance. Partial portal vein ligation resulted in vasodilation on day 3 after surgery in the water-treated rats, an effect that was prevented by treatment with phenobarbital. These results support previous suggestions that a reduction in liver function triggers renal Na(+) retention in this model. Vasodilation is not necessary for the latter effect, but also appears to be dependent on a reduction in liver function.[1]References
- Influence of phenobarbital on changes in Na(+) handling, hemodynamics and liver function due to partial portal vein ligation in rats. Sabra, R., Shuman, S. Eur. J. Pharmacol. (2001) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg