ROLE OF NEUTROPHILS IN ISCHEMIA-REPERFUSION-INDUCED MICROVASCULAR INJURY
ROLE OF NEUTROPHILS IN ISCHEMIA-REPERFUSION-INDUCED MICROVASCULAR INJURY
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DOI：
10.1152/ajpheart.1987.253.3.h699
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发表时间：
1987-09-01
影响因子：
--
通讯作者：
GRANGER, DN
中科院分区：
文献类型：
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作者：
HERNANDEZ, LA;GRISHAM, MB;GRANGER, DN
最近的研究表明，多形核中性粒细胞（PMNs）在缺血和再灌注后浸润肠黏膜。为了确定PMNs是否介导缺血再灌注（I/R）引起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。β的单克隆抗体治疗猫。CD18复合物的-链（MoAb 60.3），阻止中性粒细胞粘附和外渗。在对照制剂中测定肠微血管对血浆蛋白的通透性(0.08。0.007)，在缺血再灌注1h的制剂中(I/R, 0.32 .+-。0.02)， ANS处理的I/R制剂(0.13 .+-。0.01)，而用MoAb处理的I/R制剂(0.12 +-。0.003)。我们的研究结果表明，PMN的消耗（低于10%的对照）和PMN粘附的预防都显著减弱了I/R引起的微血管通透性的增加。这些发现，加上先前从该模型中获得的结果，支持了中性粒细胞的假设，中性粒细胞在黄嘌呤氧化酶激活的反应中积聚在粘膜中，介导了缺血肠再灌注产生的氧自由基依赖性损伤。
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 < 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.