Browicz-Kupffer cells are supposed to be the origin for free oxygen radicals, which are responsible for liver reperfusion injuries. Prostaglandin E1 prevents neutrophil activation and has a beneficial effect in acute liver atrophy and primary graft insufficiency. The aim of this study was to determine the influence of exogenous PGE1 on the extent of liver injury, following 90 minutes of its experimental ischemia by means of a temporary porto-caval anastomosis in adult Spraque-Dawley rats. The observation period lasted 24 hours. We estimated serum enzymatic markers of liver injury and performed histochemical analyses of SDH, G-6-P-ase, LDH, ATP-ase Mg, and AcP. We measured the microsomal fractions of cytochromes P-450 and b5 as well as cooperating reductases. The administration of the drug led to a significant reduction of AST, ALT, and LDH blood levels, decreased the liver tissues necrotic area and stabilized the architecture of hepatocytes. The cytoprotective effect of PGE1 was more measurable when administrated following the restoration of circulation which demonstrates the drugs influence on mechanisms initiated during the reperfusion period.

Keywords: prostaglandin E1, Ischemia-Reperfusion Injury, Liver