Neutrophil-mediated vascular injury.

Neutrophil-mediated vascular injury.
复制标题

DOI:
10.1111/j.0954-6820.1987.tb09912.x
复制
发表时间:
2009-04
期刊:
Acta medica Scandinavica. Supplementum
影响因子:
--
通讯作者:
J. Harlan
J. Harlan
中科院分区:
其他
文献类型:
--
作者:
J. Harlan

文献摘要

被引文献

相似文献

急性炎症反应的特点是增加中性粒细胞粘附内皮。许多研究者提出炎症部位的中性粒细胞积累与随后引起局部水肿、血栓形成或出血的血管损伤之间存在因果关系。中性粒细胞在急性血管损伤发病机制中起关键作用的证据来自实验研究,实验研究使用的是通过特异性抗体或化疗药物耗尽循环中性粒细胞的动物。中性粒细胞耗竭可减轻与Arthus和Shwartzman反应(1)、血清病(2)、肾毒性肾炎(3)、急性免疫性关节炎(4)、趋化素诱导的皮肤病变(3)和心肌缺血再灌注损伤(6)相关的血管损伤。急性肺损伤通常伴有中性粒细胞的肺隔离,在一些模型中,肺损伤因先前的中性粒细胞耗竭而减弱(7)。根据这些观察结果,我们似乎可以合理地假设,在某些情况下,中性粒细胞粘附在炎症部位的血管壁上并释放有毒产物,损害邻近的内皮细胞或改变内皮细胞的功能。图1总结了中性粒细胞介导的血管损伤模式。内皮作为一个“无辜的旁观者”被活化的中性粒细胞损伤,与多种临床疾病,特别是成人呼吸窘迫综合征的血管损伤的发病机制有关。
The acute inflammatory response is characterized by increased neutrophil adherence to endothelium. Many investigators have proposed a causal relationship between neutrophil accumulation at sites of inflammation and subsequent vascular injury resulting in local edema, thrombosis or hemorrhage. Evidence for a critical role of neutrophils in the pathogenesis of acute vascular injury comes from experimental studies using animals depleted of circulating neutrophils by specific antibody or chemotherapeutic agents. Neutrophil depletion attenuates vascular injury associated with the Arthus and Shwartzman reactions (l), serum sickness (2), nephrotoxic nephritis (3), acute immunologic arthritis (4), chemotaxin-induced skin lesions (3, and ischemia-reperfusion injury of the myocardium (6). Acute lung injury is often accompanied by pulmonary sequestration of neutrophils and in several models lung injury is attenuated by prior neutrophil depletion (7). From these observations it seems reasonable to hypothesize that, under some circumstances, neutrophils adhere to the vessel wall at sites of inflammation and release toxic products that damage the adjacent endothelium or alter endothelial function. This paradigm of neutrophil-mediated vascular injury is summarized in Fig. 1. Injury of endothelium as an'innocent bystander'by activated neutrophils has been implicated in the pathogenesis of vascular damage in a variety of clinical disorders, particularly the Adult Respiratory Distress Syndrome.