Hernandez L A, Grisham M B, Twohig B, Arfors K E, Harlan J M, Granger D N
Am J Physiol. 1987 Sep;253(3 Pt 2):H699-703. doi: 10.1152/ajpheart.1987.253.3.H699.
Recent studies indicate that polymorphonuclear neutrophils (PMNs) infiltrate the intestinal mucosa during ischemia and after reperfusion. To determine whether PMNs mediate the increased microvascular permeability produced by ischemia-reperfusion (I/R) we treated cats with either saline, antineutrophil serum (ANS), or a monoclonal antibody specific for the beta-chain of the CD18 complex (MoAb 60.3) that prevents neutrophil adherence and extravasation. Intestinal microvascular permeability to plasma proteins was measured in control preparations (0.08 +/- 0.007), in preparations subjected to 1 h of ischemia then reperfusion (I/R, 0.32 +/- 0.02), I/R preparations treated with ANS (0.13 +/- 0.01), and I/R preparations treated with MoAb (0.12 +/- 0.003). Our results indicate that both PMN depletion (to less than 10% control) and prevention of PMN adherence significantly attenuate the increased microvascular permeability induced by I/R. These findings, coupled to previous results obtained from this model, support the hypothesis that neutrophils, which accumulate in the mucosa in response to xanthine oxidase activation, mediate the oxyradical-dependent injury produced by reperfusion of the ischemic bowel.
最近的研究表明，多形核中性粒细胞（PMNs）在缺血期间和再灌注后会浸润肠黏膜。为了确定PMNs是否介导了缺血再灌注（I/R）所导致的微血管通透性增加，我们用生理盐水、抗中性粒细胞血清（ANS）或针对CD18复合物β链的单克隆抗体（MoAb 60.3，可防止中性粒细胞黏附和渗出）对猫进行治疗。在对照制剂（0.08±0.007）、经历1小时缺血然后再灌注的制剂（I/R，0.32±0.02）、用ANS治疗的I/R制剂（0.13±0.01）以及用MoAb治疗的I/R制剂（0.12±0.003）中测量肠微血管对血浆蛋白的通透性。我们的结果表明，PMN耗竭（至低于对照的10%）和防止PMN黏附均能显著减轻I/R诱导的微血管通透性增加。这些发现，再加上从该模型获得的先前结果，支持了这样的假说：即因黄嘌呤氧化酶激活而在黏膜中积聚的中性粒细胞介导了缺血肠再灌注所产生的氧自由基依赖性损伤。
