Kurokawa T, Nonami T, Harada A, Nakao A, Takagi H
Department of Surgery II, Nagoya University School of Medicine, Japan.
Semin Surg Oncol. 1996 May-Jun;12(3):179-82. doi: 10.1002/(SICI)1098-2388(199605/06)12:3<179::AID-SSU6>3.0.CO;2-4.
Interruption of liver blood flow is often necessary as an operative technique in liver surgery. However, this procedure causes liver damage and can be a factor in postoperative liver failure. Interruption of oxygen and substrate supply and accumulation of metabolites contribute to a great variety of cellular and subcellular dysfunctions. Impairment of liver microcirculation occurs after reperfusion. It has been presumed that there is an imbalance between the activities of vasoconstrictors and vasodilators which would determine the vascular condition during ischemia and reperfusion phases. Some mediators are known to act as cytotoxic factors, especially after reperfusion following ischemia. The phenomenon in which organ damage becomes worse, even after reperfusion, is called reperfusion injury. Mediators released from accumulated polymorphonuclear neutrophils and activated Kupffer cells such as oxygen radicals and inflammatory cytokines are associated with ischemia-reperfusion injury of the liver. Regulation of these mediators will be a therapeutic necessity for this kind of liver injury in the future.
在肝脏手术中，作为一种手术技术，肝脏血流阻断常常是必要的。然而，这一操作会导致肝损伤，并且可能是术后肝衰竭的一个因素。氧和底物供应的中断以及代谢产物的蓄积会导致各种各样的细胞和亚细胞功能障碍。再灌注后会出现肝脏微循环受损。据推测，血管收缩剂和血管舒张剂的活性之间存在失衡，这将决定缺血和再灌注阶段的血管状况。已知一些介质可作为细胞毒性因子，尤其是在缺血后的再灌注期。即使在再灌注后器官损伤仍会加重的现象称为再灌注损伤。从聚集的多形核中性粒细胞和活化的库普弗细胞释放的介质，如氧自由基和炎性细胞因子，与肝脏的缺血再灌注损伤有关。对这些介质的调控将是未来治疗这类肝损伤的必要手段。
