Trauma-hemorrhagic shock-induced up-regulation of endothelial cell adhesion molecules is blunted by mesenteric lymph duct ligation.

Abstract

Previous studies have shown that mesenteric lymph duct ligation prevents trauma-hemorrhagic shock-induced lung injury and neutrophil activation. Since endothelial cells rapidly express adhesion molecules, such as P-selectin and intercellular adhesion molecule-1, after shock, and because trauma-hemorrhagic shock-induced lung injury appears to involve neutrophil-endothelial cell interactions, we tested the hypothesis that lymph duct ligation would diminish trauma-hemorrhagic shock-induced P-selectin and intercellular adhesion molecule-1 expression in the lung and other organs. Prospective animal study with concurrent control. Small animal laboratory. Adult male Sprague-Dawley rats. Four groups of male rats were studied: trauma (laparotomy) plus sham shock, trauma-sham shock plus lymph duct ligation, trauma-hemorrhagic shock (90 mins of shock at 30 mm Hg), and trauma-hemorrhagic shock plus lymph duct ligation. At 3 or 24 hrs after trauma-hemorrhagic shock or trauma-sham shock, lung, heart, liver, kidney, intestinal, and other visceral concentrations of P-selectin and intercellular adhesion molecule-1 expression were measured using the dual radiolabeled monoclonal antibody technique. At 3 and 24 hrs, trauma-hemorrhagic shock increased endothelial cell P-selectin and intercellular adhesion molecule-1 adhesion molecule expression in the lung and liver. At 3 and 24 hrs after trauma-hemorrhagic shock, intercellular adhesion molecule-1 expression was increased in the heart, spleen, pancreas, intestine, and kidney, whereas at 24 hrs, but not 3 hrs, P-selectin expression also was increased in these organs. Lymph duct ligation prevented trauma-hemorrhagic shock-induced increased adhesion molecule expression in all of these organs with the exception of intestinal P-selectin expression. Trauma-hemorrhagic shock-induced increases in endothelial cell P-selectin and intercellular adhesion molecule-1 expression in the lung and liver as well as other tissues appear to be related to factors liberated from the ischemic gut and carried in intestinal lymph.