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Effect of isolated portal hypertension on Kupffer cell function
M H Basista1, R E Stauber, D H Van Thiel
1Division of Gastroenterology, University of Pittsburgh, Pennsylvania.
Digestive Diseases and Sciences
|January 1, 1994
Summary
Portosystemic shunting (PSS) in cirrhosis redirects pathogens away from the liver, increasing infection risk. This study shows PSS alters pathogen distribution to the periphery, even without liver cell damage.
Area of Science:
- Hepatology
- Immunology
- Surgical Pathophysiology
Background:
- Cirrhosis patients have increased infection rates, potentially due to impaired reticuloendothelial system (RES) function.
- Portosystemic shunting (PSS) in cirrhosis may compromise RES by diverting pathogens from Kupffer cells in the liver.
Purpose of the Study:
- To investigate the effect of PSS alone on RES function using a model of portal hypertension without hepatic parenchymal damage.
- To evaluate the distribution of immunologically inert particles and live bacteria in the presence of PSS.
Main Methods:
- A partial portal vein ligation (PVL) rat model was used to induce PSS without liver cell damage.
- Rats received either [99mTc]sulfur colloid or E. coli via the ileocolic vein.
- Radioactivity and bacterial counts were measured in excised organs (femur, lungs, liver, spleen).
Main Results:
- PVL rats showed significantly higher distribution of [99mTc]sulfur colloid in the lungs, spleen, and femur compared to sham-operated rats.
- PVL rats had significantly more E. coli in the lungs, but not the spleen, compared to sham rats.
- These findings indicate PSS alters RES function by increasing peripheral pathogen distribution.
Conclusions:
- PSS, independent of Kupffer cell dysfunction, alters RES function.
- The altered distribution of pathogens to the periphery may contribute to increased infection susceptibility in cirrhotic patients.
- This study highlights the role of altered hemodynamics in compromising host defense in cirrhosis.