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The relationship between neutrophils and increased microvascular permeability in a model of myocardial ischaemia and reperfusion in the rabbit.

机译:在兔心肌缺血和再灌注模型中中性粒细胞与微血管通透性增加之间的关系。

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摘要

1. 111In-labelled neutrophils and 125I-labelled albumin were used to measure neutrophil accumulation and microvascular plasma protein leakage in the ischaemic/reperfused myocardium of anaesthetized rabbits. 2. A period of 30 min coronary artery occlusion followed by 3 h reperfusion resulted in an increase in both 111In and 125I counts in the area at risk (AR) of the myocardium. 3. Pretreatment of 111In-neutrophils in vitro with monoclonal antibody 60.3 directed against the CD18 antigen on neutrophils, followed by intravenous administration, significantly suppressed their accumulation into the AR myocardium. 4. Depletion of circulating neutrophils by use of anti-neutrophil serum or mustine hydrochloride did not affect plasma protein leakage into the AR myocardium. 5. Administration of the platelet activating factor (PAF) antagonist WEB 2086 (10 mg kg-1, i.v.) had no effect on the accumulation of 111In-neutrophils or on plasma protein leakage in the AR myocardium.
机译:1. 111In标记的中性粒细胞和125I标记的白蛋白用于测量麻醉兔缺血/再灌注心肌中的中性粒细胞积累和微血管血浆蛋白渗漏。 2.一段30分钟的冠状动脉闭塞继之以3小时的再灌注,导致心肌高危区域(AR)的111In和125I计数均增加。 3.用针对中性粒细胞上的CD18抗原的单克隆抗体60.3体外预处理111In中性粒细胞,然后静脉内给药,显着抑制了它们在AR心肌中的蓄积。 4.通过使用抗中性粒细胞血清或盐酸芥子碱耗尽循环中性粒细胞不会影响血浆蛋白渗入AR心肌。 5.施用血小板活化因子(PAF)拮抗剂WEB 2086(10mg kg-1,i.v。)对111 In-中性粒细胞的积累或AR心肌中血浆蛋白的泄漏没有影响。

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