Induction of adhesion molecule expression in liver ischaemia-reperfusion injury is associated with impaired hepatic parenchymal microcirculation.

Abstract

Activated neutrophils may be important mediators in liver ischaemia-reperfusion injury (I/R). Adhesion of leucocytes to the endothelial cell surface is a result of activation of cell adhesion molecules. The aim of this study was to investigate the effect of I/R on the hepatic microcirculation (HM) and intercellular adhesion molecule (ICAM) 1 expression. Four groups of six Sprague-Dawley rats underwent laparotomy for liver exposure. Group 1 acted as controls, and groups 2-4 underwent partial liver ischaemia for 30, 45 and 60 min respectively followed by reperfusion for 60 min. Flow in the HM was measured by laser Doppler flowmetry. Liver biopsies were taken at the end of the reperfusion period. ICAM-1 expression was assessed by immunohistochemistry (graded 0-3). Mean flow in the HM was significantly reduced with I/R (mean(s.e.m.) red cell flux 140(21), 52(3) and 43(2) with 30, 45 and 60 min ischaemia compared with control 230(17); all P < 0.001). ICAM-1 expression was significantly induced (mean(s.e.m.) 1.30(0.21), 2.50(0.22) and 2.80(0.17) with 30, 45 and 60 min ischaemia versus control 0.50(0.22); all P < 0.001). I/R produced a significant upregulation of ICAM-1 expression which correlated with impaired flow in the HM.