Vedder N B, Winn R K, Rice C L, Chi E Y, Arfors K E, Harlan J M
Department of Surgery, University of Washington, Seattle 98104.
Proc Natl Acad Sci U S A. 1990 Apr;87(7):2643-6. doi: 10.1073/pnas.87.7.2643.
Tissue injury resulting from ischemia and reperfusion forms the basis of several important disorders including myocardial infarction, stroke, and circulatory shock. To examine the role of neutrophils in this process and to determine the extent to which injury is a consequence of reperfusion, we utilized the monoclonal antibody 60.3, directed to CD18, the human leukocyte adherence glycoprotein, to block intravascular neutrophil aggregation and neutrophil adherence to endothelium in a rabbit model of tissue ischemia and reperfusion. Antibody treatment either before ischemia or after ischemia, but prior to reperfusion, resulted in the same degree of significant protection against endothelial, microvascular, and tissue injury. We conclude that neutrophils and increased neutrophil adhesiveness are important in the development of microvascular and tissue injury after ischemia and reperfusion and that under these circumstances, injury is primarily a consequence of reperfusion.
缺血和再灌注导致的组织损伤是包括心肌梗死、中风和循环性休克在内的几种重要疾病的基础。为了研究中性粒细胞在此过程中的作用，并确定损伤在多大程度上是再灌注的结果，我们在兔组织缺血和再灌注模型中，使用针对人白细胞黏附糖蛋白CD18的单克隆抗体60.3来阻断血管内中性粒细胞聚集以及中性粒细胞与内皮的黏附。在缺血前或缺血后但在再灌注前进行抗体治疗，均可产生同等程度的显著保护作用，防止内皮、微血管和组织损伤。我们得出结论，中性粒细胞以及中性粒细胞黏附性增加在缺血和再灌注后微血管和组织损伤的发生过程中起重要作用，并且在这些情况下，损伤主要是再灌注的结果。
