INHIBITION OF LEUKOCYTE ADHERENCE BY ANTI-CD18 MONOCLONAL-ANTIBODY ATTENUATES REPERFUSION INJURY IN THE RABBIT EAR
INHIBITION OF LEUKOCYTE ADHERENCE BY ANTI-CD18 MONOCLONAL-ANTIBODY ATTENUATES REPERFUSION INJURY IN THE RABBIT EAR
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DOI：
10.1073/pnas.87.7.2643
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发表时间：
1990-04-01
影响因子：
11.1
通讯作者：
HARLAN, JM
中科院分区：
文献类型：
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作者：
VEDDER, NB;WINN, RK;HARLAN, JM
缺血和再灌注引起的组织损伤是几种重要疾病的基础，包括心肌梗死、中风和循环性休克。为了研究中性粒细胞在这一过程中的作用并确定再灌注损伤的程度，我们利用针对人白细胞黏附糖蛋白CD18的单抗60.3在兔组织缺血再灌流模型中阻断血管内中性粒细胞聚集和中性粒细胞与内皮的黏附。无论是在缺血前还是在缺血后，但在再灌流之前，抗体治疗都能对内皮、微血管和组织损伤产生相同程度的显著保护。我们得出结论，中性粒细胞和增加的中性粒细胞粘附性在缺血和再灌流后微血管和组织损伤的发展中起重要作用，在这种情况下，损伤主要是再灌流的结果。
Tissue injury resulting forms 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 processed 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 imporant in the development of microvascular and tissue injury after ischemia and reperfusion and that under these circumstances, injury is primarily a consequence of reperfusion.