Department of Neurological Surgery, Columbia University, New York, NY 10032, USA.
Mediators Inflamm. 2009;2009:124384. doi: 10.1155/2009/124384. Epub 2010 Jan 26.
Out-of-hospital cardiac arrest (OHCA) is a devastating disease process with neurological injury accounting for a disproportionate amount of the morbidity and mortality following return of spontaneous circulation. A dearth of effective treatment strategies exists for global cerebral ischemia-reperfusion (GCI/R) injury following successful resuscitation from OHCA. Emerging preclinical as well as recent human clinical evidence suggests that activation of the complement cascade plays a critical role in the pathogenesis of GCI/R injury following OHCA. In addition, it is well established that complement inhibition improves outcome in both global and focal models of brain ischemia. Due to the profound impact of GCI/R injury following OHCA, and the relative lack of effective neuroprotective strategies for this pathologic process, complement inhibition provides an exciting opportunity to augment existing treatments to improve patient outcomes. To this end, this paper will explore the pathophysiology of complement-mediated GCI/R injury following OHCA.
院外心脏骤停（OHCA）是一种具有破坏性的疾病过程，神经损伤在自主循环恢复后发病率和死亡率方面占很大比例。成功复苏 OHCA 后，针对全球脑缺血再灌注（GCI/R）损伤，目前缺乏有效的治疗策略。新出现的临床前和最近的人体临床证据表明，补体级联的激活在 OHCA 后 GCI/R 损伤的发病机制中起着关键作用。此外，众所周知，补体抑制可改善全球和局灶性脑缺血模型的预后。由于 OHCA 后 GCI/R 损伤的巨大影响，以及针对这种病理过程的相对缺乏有效神经保护策略，补体抑制为增强现有治疗方法以改善患者预后提供了一个令人兴奋的机会。为此，本文将探讨 OHCA 后补体介导的 GCI/R 损伤的病理生理学。
