Ar'Rajab A, Dawidson I, Fabia R
Department of Surgery, University of Texas, South-western Medical Center at Dallas, USA.
New Horiz. 1996 May;4(2):224-34.
Reperfusion injury, precipitated by lack of oxygen, is likely to play a major role in many clinical conditions, including shock, coronary artery occlusion disease, and solid organ transplantation. Certain tissues, such as the intestinal mucosa, may be especially susceptible because of the specific microvascular anatomy. Structural changes include not only swelling of the organelles but also the entire cell due to the entry of water and electrolytes. Lysosomal ruptures precede cell death. Other key substances which either participate in or are part of oxygen free radical formation in tissue injury are calcium ions, leukocytes, and bacteria. Leukocyte adhesion has been implicated as a critical step in vascular endothelium injury, leading to increased microvascular permeability and thrombosis. Induction of neutropenia or the administration of antileukocyte adhesion monoclonal antibodies, preventing typical injuries, implies a central role of the white blood cells in reperfusion injury. Specifically, oxygen free radical formation in the intestines may trigger or cause injury in other distant organs, e.g., the heart and lungs, and affect overall vascular function. So-called "bacterial translocation" from the intestines to the lymphatic vessels and the bloodstream is a more recently discovered phenomenon whose role is largely unknown. Ischemic preconditioning is still another concept, mainly tested in the canine heart, that has potential clinical applications. Reperfusion of ischemic tissue occurs with solid organ transplantation, often after considerable cold ischemia time. Protective mechanisms include oxygen free radical scavengers, i.e., allopurinol and superoxide dismutase. Other measures proven to be effective during the implantation are blood volume expansion with colloid solutions and/or electrolyte solutions, and the administration of a calcium antagonist. The mechanisms of these measures are likely related to improved renal microcirculation and relief of vasospasm.
由缺氧引发的再灌注损伤可能在许多临床病症中起主要作用，包括休克、冠状动脉闭塞性疾病和实体器官移植。某些组织，如肠黏膜，由于其特定的微血管解剖结构，可能特别容易受到影响。结构变化不仅包括细胞器肿胀，还包括由于水和电解质进入导致的整个细胞肿胀。溶酶体破裂先于细胞死亡。在组织损伤中参与或构成氧自由基形成一部分的其他关键物质是钙离子、白细胞和细菌。白细胞黏附被认为是血管内皮损伤的关键步骤，导致微血管通透性增加和血栓形成。诱导中性粒细胞减少或给予抗白细胞黏附单克隆抗体可预防典型损伤，这意味着白细胞在再灌注损伤中起核心作用。具体而言，肠道中氧自由基的形成可能引发或导致其他远处器官（如心脏和肺）的损伤，并影响整体血管功能。所谓的从肠道到淋巴管和血流的“细菌移位”是一种最近发现的现象，其作用在很大程度上尚不清楚。缺血预处理是另一个概念，主要在犬心脏中进行测试，具有潜在的临床应用价值。缺血组织的再灌注发生在实体器官移植时，通常是在相当长的冷缺血时间之后。保护机制包括氧自由基清除剂，即别嘌醇和超氧化物歧化酶。在植入过程中被证明有效的其他措施包括用胶体溶液和/或电解质溶液扩充血容量，以及给予钙拮抗剂。这些措施的机制可能与改善肾微循环和缓解血管痉挛有关。
