Leukocytes contribute to hepatic ischemia/reperfusion injury via intercellular adhesion molecule-1-mediated venular adherence

Leukocytes are suggested to modulate ischemia/reperfusion injury via membrane receptor-controlled interaction with the microvascular endothelium. With the use of intravital fluorescence microscopy we investigated the role of the intercellular adhesion molecule-1 (ICAM-1) in a rat model of hepatic re...

Full description

Saved in:
Bibliographic Details
Published in:Surgery 1995-02, Vol.117 (2), p.195-200
Main Authors: Vollmar, Brigitte, Glasz, Julia, Menger, Michael D., Messmer, Konrad
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Cell Adhesion
Endothelium, Vascular - pathology
Endothelium, Vascular - physiology
Gastroenterology. Liver. Pancreas. Abdomen
Immunoenzyme Techniques
Intercellular Adhesion Molecule-1 - immunology
Intercellular Adhesion Molecule-1 - physiology
Leukocytes - physiology
Liver - blood supply
Liver. Biliary tract. Portal circulation. Exocrine pancreas
Male
Medical sciences
Microscopy, Fluorescence
Other diseases. Semiology
Rats
Rats, Sprague-Dawley
Reperfusion Injury - etiology
Reperfusion Injury - pathology
Venules - pathology
Venules - physiology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Leukocytes are suggested to modulate ischemia/reperfusion injury via membrane receptor-controlled interaction with the microvascular endothelium. With the use of intravital fluorescence microscopy we investigated the role of the intercellular adhesion molecule-1 (ICAM-1) in a rat model of hepatic reperfusion injury with a neutralizing monoclonal antibody (anti-ICAM-1). Sixty minutes of left lobar ischemia and reperfusion (isotype-matched immunoglobulin G 1 control antibody) caused leukostasis in sinusoids (240±15 cells per liver lobule), leukocyte adherence in postisnusoidal venules (679±76 cells per mm 2 endothelial surface of postsinusoidal venules), nutritive perfusion failure (15%±2% nonperfused sinusoids), excretory dysfunction (bile flow, 1.2±0.3 μl·min −1·gm −1), and loss of hepatocellular integrity (serum aspartate aminotransferase, 1353±317 units·L −1; serum alanine aminotransferase, 1055±265 units·L −1). Anti-ICAM-1 did not affect sinusoidal leukostasis; however, it effectively inhibited postischemic leukocyte adherence to the venular endothelial lining (217±38 cells/mm 2, p
ISSN:0039-6060
1532-7361
DOI:10.1016/S0039-6060(05)80085-6