Menger M D, Lehr H A, Messmer K
Institut für Chirurgische Forschung, Klinikum Grosshadern, Ludwig-Maximilians-Universität München.
Klin Wochenschr. 1991 Dec 15;69(21-23):1050-5. doi: 10.1007/BF01645157.
Reperfusion after transient tissue ischemia constitutes an irrevocable need to preserve tissue viability. However, release of prolonged ischemia will either result in failure of the microcirculation to reperfusion (no-reflow) and thus the prolongation of hypoxia, or in restoration of blood flow resulting in reoxygenation of the inflicted tissue. While ischemia damages the tissue primarily through hypoxia-induced depletion of energy stores, reoxygenation paradoxically contributes to tissue damage through the formation of oxygen radicals, the release of chemoattractant mediators (TNF, IL-1, LTB4), and the activation of circulating polymorphonuclear leukocytes (PMNs). Through the action of chemoattractant mediators and the upregulation of leukocytic (CD11/CD18) and endothelial adhesion receptors (ICAM, GMP-140), activated PMNs adhere to the endothelium, release further chemoattractants and oxygen radicals and undertain a vicious circle, which will ultimately result in further tissue damage. Both the no-reflow phenomenon and the events initiated by reflow--termed herein as the reflow-paradox--contribute to the failure of the nutritive microvascular perfusion and loss of tissue viability following ischemia and reperfusion.
短暂性组织缺血后的再灌注是维持组织活力的必然需求。然而，长时间缺血的解除要么会导致微循环无法再灌注（无复流），进而延长缺氧时间，要么会使血流恢复，导致受损组织再氧合。缺血主要通过缺氧诱导的能量储备耗竭来损伤组织，而与之相悖的是，再氧合会通过氧自由基的形成、趋化介质（肿瘤坏死因子、白细胞介素 -1、白三烯B4）的释放以及循环多形核白细胞（PMN）的激活来加剧组织损伤。通过趋化介质的作用以及白细胞（CD11/CD18）和内皮黏附受体（细胞间黏附分子、血小板 - 内皮细胞黏附分子 -140）的上调，活化的PMN黏附于内皮，释放更多趋化因子和氧自由基，从而形成恶性循环，最终导致进一步的组织损伤。无复流现象以及由再灌注引发的一系列事件（本文称之为再灌注悖论），均会导致缺血再灌注后营养性微血管灌注失败和组织活力丧失。
