Dai C L, Kume M, Yamamoto Y, Yamagami K, Yamamoto H, Nakayama H, Ozaki N, Shapiro A M, Yamamoto M, Yamaoka Y
Department of Gastroenterological Surgery, Kyoto University Graduate School of Medicine, Sakyo, Japan.
Br J Surg. 1998 Aug;85(8):1061-5. doi: 10.1046/j.1365-2168.1998.00771.x.
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.
肝缺血再灌注损伤的发病机制尚未完全明确。本研究通过监测大鼠肝组织中热休克蛋白（HSP）72的产生，探讨门静脉淤血再灌注对普林格尔手法（Pringle's manoeuvre）后肝脏缺血再灌注损伤的影响。
将大鼠随机分为三组。第1组通过普林格尔手法诱导肝缺血并伴有门静脉淤血15分钟；第2组采用普林格尔手法15分钟并建立体外门体分流；第3组肠系膜上静脉阻断15分钟。每次干预后48小时，通过蛋白质免疫印迹法检测肝组织中HSP72的产生。再灌注后1、3和48小时检测肝功能的常规参数。
第1组有明显的HSP72表达，而第2组和第3组没有，表明肝缺血和门静脉淤血再灌注相结合才能诱导组织中HSP72的强烈表达。另一方面，第1组和第2组的生化参数均同等升高，反映出缺血性肝细胞损伤程度相似。
本研究通过原位肝HSP72的产生清楚地检测到了临时门静脉阻断对肝脏缺血再灌注损伤的额外应激影响。
