Role of Microcirculatory Derangements in Manifestation of Portal Triad Cross-Clamping-Induced Hepatic Reperfusion Injury

Postischemic liver dysfunction following portal triad cross-clamping (PTC) predisposes patients for the development of multiple system organ failure (MSOF) and is associated with increased mortality of MSOF. The deterioration of the hepatic microcirculation may play a pivotal role in the pathophysio...

Full description

Saved in:
Bibliographic Details
Published in:The Journal of surgical research 1996-01, Vol.60 (1), p.49-54
Main Authors: Vollmar, Brigitte, Glasz, Julia, Post, Stefan, Menger, Michael D.
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Constriction
Gastroenterology. Liver. Pancreas. Abdomen
Hemodynamics
Ischemia - pathology
Ischemia - physiopathology
Liver - blood supply
Liver - pathology
Liver - physiopathology
Liver Circulation
Liver. Biliary tract. Portal circulation. Exocrine pancreas
Male
Medical sciences
Microcirculation
Other diseases. Semiology
Portal System
Rats
Rats, Sprague-Dawley
Reperfusion Injury - pathology
Reperfusion Injury - physiopathology
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Postischemic liver dysfunction following portal triad cross-clamping (PTC) predisposes patients for the development of multiple system organ failure (MSOF) and is associated with increased mortality of MSOF. The deterioration of the hepatic microcirculation may play a pivotal role in the pathophysiologic sequelae of PTC-induced reperfusion injury. We quantitatively analyzedin vivothe role of microcirculatory derangements in the manifestation of hepatic reperfusion injury following ischemia by PTC. Sprague–Dawley rats were subjected to 20 min PTC followed by 60 min reperfusion (PTC,n= 18). Sham-operated animals without ischemia served as controls (sham,n= 15). Within 45–60 min of reperfusion, hepatic microcirculation (sinusoidal perfusion, leukocyte–endothelial cell interaction) was analyzed by means of intravital fluorescence microscopy; tissue oxygenation was assessed using a platinum multiwire surface electrode. Liver enzymes and bile flow were determined as indicators of hepatocellular integrity and liver function.In vivoanalysis of postischemic hepatic microcirculation revealed the induction of leukocyte–endothelial cell interaction within sinusoids and postsinusoidal venules and concomitant sinusoidal perfusion deficits associated with tissue hypoxia. In addition, PTC resulted in increased serum levels of liver enzymes and a marked reduction of bile flow. Regression analyses demonstrated significant correlations between hepatocellular desintegration/liver dysfunction and PTC-induced microcirculatory disorders. These results underline the predominant role of microcirculatory disturbances in the development of PTC-induced hepatic reperfusion injury and support the concept that normalization of postischemic microcirculation may be a most effective therapeutic regimen to prevent hepatocellular damage and liver dysfunction.
ISSN:0022-4804
1095-8673
DOI:10.1006/jsre.1996.0009