Hearse D J
Rayne Institute, St. Thomas' Hospital, London, UK.
Cardiovasc Drugs Ther. 1991 Mar;5 Suppl 2:225-35. doi: 10.1007/BF00054745.
While some investigators recognize "reperfusion-induced injury" as an important component of the overall injury that occurs during ischemia and reperfusion, others question its existence. Resolution of this controversy is of considerable importance, particularly in an era of thrombolysis, since reperfusion-induced injury might be amenable to treatment. Although reperfusion is an absolute prerequisite for the recovery of ischemic tissue, it undoubtedly has some unfavorable effects. The identification of four (possibly sequential) components of reperfusion-induced injury helps to clarify the situation: a) Reperfusion after brief periods of ischemia can trigger arrhythmias in tissue that is potentially salvable; there is abundant experimental and clinical evidence for this form of reperfusion injury. b) Reperfusion may also be associated with "myocardial stunning"; however, given sufficient time, this prolonged postischemic contractile and metabolic dysfunction will recover. There is good experimental evidence and some clinical evidence for the existence of this type of reperfusion-induced injury. c) Reperfusion is commonly thought to cause lethal injury in cells that, until the time of reperfusion, were potentially salvable. However, conclusive evidence that reperfusion can kill cells does not yet exist. d) Reperfusion may alter the nature of necrotic processes in tissue that has already sustained lethal injury, while not altering the number of cells that die this may change the manner in which they die; this form of reperfusion injury could lead to differences in scar formation and vulnerability to aneurysm. There is considerable evidence for the existence of this form of reperfusion-induced injury. Many candidate mechanisms have been proposed for each form of reperfusion injury. Ionic disturbances (particularly for calcium) are often cited and, most recently, free radical-induced induced injury (oxidant stress) has been suggested as important. Considerable evidence exists that oxidant stress is involved in stunning and in reperfusion-induced arrhythmias, and characterization of underlying mechanisms might lead to novel therapeutic principles, such as antioxidant therapy. However, much remains to be learned.
虽然一些研究人员认为“再灌注诱导损伤”是缺血再灌注期间发生的整体损伤的一个重要组成部分，但另一些人则对其存在表示质疑。解决这一争议相当重要，尤其是在溶栓时代，因为再灌注诱导损伤可能适合治疗。尽管再灌注是缺血组织恢复的绝对前提，但它无疑有一些不利影响。对再灌注诱导损伤的四个（可能是相继的）组成部分的识别有助于阐明情况：a）短暂缺血后的再灌注可在有潜在挽救可能的组织中引发心律失常；这种形式的再灌注损伤有丰富的实验和临床证据。b）再灌注也可能与“心肌顿抑”有关；然而，给予足够时间，这种缺血后延长的收缩和代谢功能障碍将会恢复。这种类型的再灌注诱导损伤的存在有充分的实验证据和一些临床证据。c）通常认为再灌注会在直到再灌注时仍有潜在挽救可能的细胞中造成致命损伤。然而，尚无确凿证据表明再灌注会杀死细胞。d）再灌注可能会改变已经遭受致命损伤的组织中坏死过程的性质，虽然不会改变死亡细胞的数量，但可能会改变它们死亡的方式；这种形式的再灌注损伤可能导致瘢痕形成和动脉瘤易感性的差异。有大量证据表明这种形式的再灌注诱导损伤存在。针对每种形式的再灌注损伤都提出了许多候选机制。离子紊乱（特别是钙）经常被提及，最近，自由基诱导的损伤（氧化应激）也被认为很重要。有大量证据表明氧化应激与顿抑和再灌注诱导的心律失常有关，对潜在机制的表征可能会导致新的治疗原则，如抗氧化治疗。然而，仍有许多有待了解的地方。
