*Institute for Molecular Bioscience and †School of Biomedical Sciences, The University of Queensland, Brisbane, Queensland, Australia.
Shock. 2013 Dec;40(6):463-70. doi: 10.1097/SHK.0000000000000044.
Ischemia-reperfusion injury (IRI) is a common occurrence following myocardial infarction, transplantation, stroke, and trauma that can lead to multiple organ failure, which remains the foremost cause of death in critically ill patients. Current therapeutic strategies for IRI are mainly palliative, and there is an urgent requirement for a therapeutic that could prevent or reverse tissue damage caused by IRI. Neutrophils are the primary responders following ischemia and reperfusion and represent important components in the protracted inflammatory response and severity associated with IRI. Experimental studies demonstrate neutrophil infiltration at the site of ischemia and show that inducing neutropenia can protect organs from IRI. In this review, we highlight the mechanisms involved in neutrophil recruitment, activation, and adherence and how this contributes to disease severity in IRI. Inhibiting neutrophil mobilization, tissue recruitment, and ultimately neutrophil-associated activation of local and systemic inflammatory responses may have therapeutic potential in the amelioration of local and remote tissue damage following IRI.
缺血再灌注损伤（IRI）是心肌梗死、移植、中风和创伤后常见的现象，可导致多器官衰竭，这仍然是危重病患者死亡的首要原因。目前针对 IRI 的治疗策略主要是姑息性的，迫切需要一种能够预防或逆转 IRI 引起的组织损伤的治疗方法。中性粒细胞是缺血和再灌注后的主要反应细胞，是与 IRI 相关的慢性炎症反应和严重程度的重要组成部分。实验研究表明中性粒细胞在缺血部位的浸润，并表明诱导中性粒细胞减少症可保护器官免受 IRI 的损伤。在这篇综述中，我们强调了中性粒细胞募集、激活和黏附的机制，以及这如何导致 IRI 中的疾病严重程度。抑制中性粒细胞的动员、组织募集，以及最终中性粒细胞相关的局部和全身炎症反应的激活，可能在改善 IRI 后局部和远处组织损伤方面具有治疗潜力。
