Jaeschke H
Department of Pharmacology, Pharmacia & Upjohn, Inc., 301 Henrietta Street, Kalamazoo, MI 49007, USA.
J Hepatobiliary Pancreat Surg. 1998;5(4):402-8. doi: 10.1007/s005340050064.
The review highlights recent advances in our understanding of basic mechanisms of reperfusion injury after warm hepatic ischemia. Kupffer cells play a central role as the initial cytotoxic cell type and as a source of many proinflammatory mediators. Subsequently, neutrophils are activated and recruited into the liver. Factors and conditions are outlined that determine whether neutrophils undergo apoptosis without causing damage or migrate out of the sinusoids and attack parenchymal cells. In addition to the inevitable inflammatory response during reperfusion, microcirculatory perfusion failure, due to an imbalance between the actions of vasodilators and vasoconstrictors, also has a serious impact on reperfusion injury. A better understanding of the basic pathophysiology will reveal potential targets for therapeutic interventions and will show us how to avoid risk factors that may aggravate reperfusion injury.
这篇综述重点介绍了我们对热缺血后肝脏再灌注损伤基本机制理解的最新进展。库普弗细胞作为初始细胞毒性细胞类型以及多种促炎介质的来源发挥着核心作用。随后，中性粒细胞被激活并募集到肝脏中。文中概述了决定中性粒细胞是发生凋亡而不造成损伤还是从肝血窦迁移出来并攻击实质细胞的因素和条件。除了再灌注过程中不可避免的炎症反应外，血管舒张剂和血管收缩剂作用失衡导致的微循环灌注衰竭，也对再灌注损伤有严重影响。更好地理解基本病理生理学将揭示治疗干预的潜在靶点，并向我们展示如何避免可能加重再灌注损伤的危险因素。
