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

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

doi:10.1016/0022-4804(91)90184-N

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

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

Research output: Contribution to journal › Article › peer-review

19 Scopus citations

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 language	English (US)
Pages (from-to)	234-239
Number of pages	6
Journal	Journal of Surgical Research
Volume	50
Issue number	3
DOIs	https://doi.org/10.1016/0022-4804(91)90184-N
State	Published - Mar 1991

ASJC Scopus subject areas

Surgery

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title = "Contribution of portal systemic shunt to Kupffer cell dysfunction in obstructive jaundice",

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.",

author = "Dunn, {Charles W.} and Horton, {Jureta W.} and Megison, {Stephen M.} and Vuitch, {M. Franklin}",

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AU - Dunn, Charles W.

AU - Horton, Jureta W.

AU - Megison, Stephen M.

AU - Vuitch, M. Franklin

PY - 1991/3

Y1 - 1991/3

N2 - 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.

AB - 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.

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

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