Multiple organ dysfunction syndrome (
MODS) is mediated by complex mechanisms in which interactions between activated leukocytes and endothelial cells play a central role.
ICAM-1 (
intercellular adhesion molecule-1) mediates firm adhesion and transendothelial migration of activated leukocytes from postcapillary venules into the tissue. The present study evaluated the
ICAM-1 expression in various organs after 40 min of intestinal
ischemia and 1, 3, 6, 12 h of reperfusion (I/R) in the rat, using a dual
monoclonal antibody technique (n = 36). Endothelial barrier permeability, using the vascular leakage of radiolabeled
human serum albumin was also assessed (n = 12). Neutrophil sequestration in the lungs was quantitated by
myeloperoxidase activity and plasma
protease inhibitor levels were measured with electroimmunoassay. Significant regional differences were found in
ICAM-1 expression between organs, both constitutively and after I/R-injury. The highest constitutive levels were observed in the liver and lungs, followed by the kidneys. The constitutive
ICAM-1 expression in the intestines and in the heart was about 1/20 compared with that found in the liver and lungs. The brain and muscle had levels of about 1/150 of that in the liver and lungs. After intestinal I/R, significant increases (17-45%) were found in the lungs, intestines, brain, heart, and muscle.
Albumin leakage index (ALI) in all examined organs and
myeloperoxidase activity in the lungs increased after I/R-injury. Serum levels of
albumin and most
protease inhibitors decreased significantly after I/R challenge. Intestinal I/R results in an increase of systemic
ICAM-1 expression with marked organ variability. The upregulation of
ICAM-1 could represent a crucial step in the adherence- and migration process of activated leukocytes and potentially in the development of tissue injury.