Neutrophil-mediated vascular injury.
Neutrophil-mediated vascular injury.
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DOI:
10.1111/j.0954-6820.1987.tb09912.x
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发表时间:
2009-04
期刊:
影响因子:
--
通讯作者:
J. Harlan
中科院分区:
文献类型:
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作者:
J. Harlan
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.