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对肺缺血-再灌注损伤的炎症反应。

Inflammatory response to pulmonary ischemia-reperfusion injury.

作者信息

Ng Calvin S H, Wan Song, Arifi Ahmed A, Yim Anthony P C

机构信息

Division of Cardiothoracic Surgery, The Chinese University of Hong Kong, Prince of Wales Hospital, Sha Tin, NT, Hong Kong, China.

出版信息

Surg Today. 2006;36(3):205-14. doi: 10.1007/s00595-005-3124-2.

Abstract

Lung ischemia-reperfusion (IR) injury is one of the most important complications following lung transplant and cardiopulmonary bypass. The pulmonary dysfunction following lung IR has been well documented. Recent studies have shown that ischemia and reperfusion of the lung may each play significant yet differing roles in inducing lung injury. The mechanisms of injury involving neutrophil activation, and the release of numerous inflammatory mediators and oxygen radicals also contributes to lung cellular injury, pneumocyte necrosis, and apoptosis. We herein review the current understanding of the underlying mechanism involved in lung IR injury. The biomolecular mechanisms and interactions which lead to the inflammatory response, pneumocyte necrosis, and apoptosis following lung IR therefore warrant further investigation.

摘要

肺缺血再灌注(IR)损伤是肺移植和体外循环后最重要的并发症之一。肺IR后的肺功能障碍已有充分记录。最近的研究表明,肺的缺血和再灌注在诱导肺损伤中可能各自发挥重要但不同的作用。涉及中性粒细胞活化以及多种炎症介质和氧自由基释放的损伤机制也导致肺细胞损伤、肺细胞坏死和凋亡。我们在此回顾目前对肺IR损伤潜在机制的理解。因此,导致肺IR后炎症反应、肺细胞坏死和凋亡的生物分子机制及相互作用值得进一步研究。

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