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Tissue eicosanoids and vascular permeability in rats with chronic biliary obstruction
N Ohara1, N F Voelkel, S W Chang
1Cardiovascular Pulmonary Research Laboratory, University of Colorado Health Sciences Center, Denver 80262.
Hepatology (Baltimore, Md.)
|July 1, 1993
Summary
Advanced cirrhosis increases albumin leakage in rat lungs and kidneys. Thromboxane A2 contributes to lung vascular permeability, but its role in kidney leakage requires further investigation.
Area of Science:
- Hepatology
- Vascular Biology
- Pharmacology
Background:
- Advanced cirrhosis is linked to extrahepatic organ dysfunction.
- The underlying mechanisms of this complication remain largely unknown.
Purpose of the Study:
- To investigate the role of arachidonic acid metabolites in vascular permeability changes associated with cirrhosis.
- To determine the contribution of thromboxane A2 to organ dysfunction in biliary cirrhosis and cholestasis.
Main Methods:
- Measuring 125I-albumin leakage in rat tissues (lung, kidney, heart, brain) after bile duct ligation.
- Quantifying tissue thromboxane B2 levels using enzyme immunoassay.
- Administering the thromboxane synthase inhibitor dazoxiben to assess its effect on vascular permeability.
Main Results:
- Biliary cirrhotic rats showed increased albumin leakage in the lung and kidney.
- Cholestatic rats exhibited increased albumin leakage primarily in the kidney.
- Thromboxane B2 levels were elevated in the lung, kidney, and liver of both cirrhotic and cholestatic rats.
- Dazoxiben reduced lung thromboxane B2 levels and albumin leakage, suggesting thromboxane A2's role in lung permeability.
Conclusions:
- Chronic biliary obstruction in rats increases vascular permeability in specific extrahepatic organs.
- Thromboxane A2 contributes to increased lung vascular permeability in cirrhosis.
- The role of thromboxane A2 in renal albumin leakage warrants further research.