Heat shock protein 72 production in liver tissue after experimental total hepatic inflow occlusion

The pathogenesis of hepatic ischaemia-reperfusion injury is incompletely understood. This study examined the effects of reperfusion with congested portal blood on ischaemia-reperfusion injury of the liver following Pringle's manoeuvre, as monitored by heat shock protein (HSP) 72 production in rat liver tissue.

Rats were randomized to three groups. In group 1 hepatic ischaemia with portal congestion was induced by Pringle's manoeuvre for 15 min; in group 2 Pringle's manoeuvre was applied for 15 min with an extracorporeal portasystemic shunt; and in group 3 the superior mesenteric vein was occluded for 15 min. The production of HSP72 in liver tissue was measured by Western blotting at 48 h after each intervention. Conventional parameters for hepatic function were examined at 1, 3 and 48 h after reperfusion.

There was marked HSP72 expression in group 1, but not in group 2 or 3, showing that a combination of liver ischaemia and reperfusion of congested portal blood is required to induce strong expression of HSP72 in the tissue. On the other hand, biochemical parameters were raised equally in both groups 1 and 2, reflecting a similar degree of ischaemic hepatocyte injury.

The additional stress impact of temporary portal occlusion upon ischaemia-reperfusion injury of the liver was clearly detected by in situ hepatic HSP72 production in this study.