Involvement of Adhesion molecules and oxygen free radicals in microcirculatory disturbance in ischemia-reperfusion injury of the liver

点击翻译按钮获取中文摘要

The AIM of this study is to investigate the involvement of adhesion molecules and oxigen free radicals in ischemia-reperfusion injury of the liver. RESULTS: [Exam 1] 1) ALT and AST were significantly decreased by PGE1 or anti ICAM-1 administration. PGE1 increased the bile production significantly. They were also decreased in neutrophil depleted rats. 2) IL-8 was not influenced by administration of PGE1 nor anti-ICAM-1 antibody. 3) The retention rate of fluorescence labeled hyaluronic acid was significantly decreased by PGE1, anti-ICAM-1 administration or in neutrophil depleted rats. [Exam 2] After reperfusion adherent leukocytes had progressively increased significantly in Control group but not in PGE1 and anti-ICAM-1 group. [Exam 3] The expression of LFA-1 and Mac-1 by flow cytometric study was not affected by PGE1. However ICAM-1 on endothelium was suppressed by PGE1 administration. [Exam 4] Oxygen free radicals derived from hepatocytes and endothelium were decreased by PGE1 administration. CONCLUSION: These data indicate that adhesion molecules plays a pivotal role in liver injury after reperfusion. Neutrophil adhesion to endothelial cells caused microcirculatory disturbance after ischemia- reperfusion. PGE1 protects against liver injury through the reduction of neutrophil-endothelial cell adhesion by supression of ICAM-1 expression.