Contribution of portal systemic shunt to Kupffer cell dysfunction in obstructive jaundice

Charles W. Dunn, Jureta W. Horton, Stephen M. Megison, M. Franklin Vuitch

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Abstract

Previous animal models of biliary tract obstruction have shown that hepatic phagocytic activity is impaired secondary to Kupffer cell dysfunction. Biliary tract obstruction leads to portal hypertension and an associated portal systemic shunt. Forty-eight Sprague-Dawley rats were studied to determine the contribution of portal systemic shunt to Kupffer cell dysfunction after 21 days of obstructive jaundice or sham operation. Liver uptake of radiolabeled Escherichia coli decreased from 76.1 ± 1.4% (sham) to 63.1 ± 6.1% in the common duct ligation (CDL) rats (P < 0.05); lung uptake increased from 4.0 ± 0.6% (sham) to 20.2 ± 4.5 (CDL) (P < 0.05). Portal systemic shunt, determined using radioactive microspheres, increased from 2.0 ± 1.0% (sham) to 46.6 ± 13.1% (CDL), P < 0.05. Although a significant portal systemic shunt does exist in this 21-day model of obstructive jaundice, it does not appear to be the only mechanism underlying Kupffer cell dysfunction.

Original languageEnglish (US)
Pages (from-to)234-239
Number of pages6
JournalJournal of Surgical Research
Volume50
Issue number3
DOIs
StatePublished - Mar 1991

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ASJC Scopus subject areas

  • Surgery

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