Inhibition of CD18-dependent adherence of polymorphonuclear leukocytes does not affect liver oxygen consumption in fecal peritonitis in pigs.

Circulatory shock Pub Date : 1993-12-01
S Wollert, I Rasmussen, C Lundberg, B Gerdin, D Arvidsson, U Haglund
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Abstract

We tested the hypothesis that circulating polymorphonuclear leukocytes (PMNs), adhering to endothelium of the liver vascular bed are involved in the alterations of the liver oxygen delivery (DO2) and consumption (VO2) that is a result of fecal peritonitis in pigs. Twenty-two pigs were divided into three groups. Animals in group I (n = 7) served as controls. Fecal peritonitis was induced in groups II (n = 7) and III (n = 8). Animals in group III were pretreated with IB4, a monoclonal anti-CD18 antibody inhibiting adherence of PMNs to the endothelium. Peritonitis increased liver VO2 in groups II and III in spite of decreased liver DO2. In group I, circulating PMNs increased during the experimental period. Sepsis caused a decrease in the number of circulating PMNs in group II, an effect that was fully counteracted in group III, where the number of PMNs rose to control level. Myeloperoxidase activity and morphometric determination of PMN infiltration in liver biopsies virtually paralleled the circulating PMN count. Although fecal peritonitis is followed by a CD18-dependent leukopenia that can be counteracted by pretreatment with an anti-CD18 antibodies, this treatment does not affect the alteration in liver VO2 and DO2 observed.

抑制cd18依赖性多形核白细胞粘附不影响猪粪便性腹膜炎的肝脏耗氧量。
我们验证了一种假设,即粘附在肝脏血管床内皮上的循环多形核白细胞(PMNs)参与了猪粪性腹膜炎导致的肝脏氧输送(DO2)和耗氧量(VO2)的改变。22头猪被分为三组。第一组(n = 7)为对照组。II组(n = 7)和III组(n = 8)诱导粪性腹膜炎。III组用IB4(一种抑制PMNs粘附内皮的单克隆抗cd18抗体)预处理。腹膜炎增加了II组和III组的肝脏VO2,尽管肝脏DO2降低。在I组,循环pmn在实验期间增加。脓毒症导致II组循环pmn数量减少,在III组完全抵消了这种影响,其中pmn数量上升到控制水平。髓过氧化物酶活性和肝活检中PMN浸润的形态测定几乎与循环PMN计数平行。虽然粪便性腹膜炎之后会出现cd18依赖性白细胞减少,可以通过抗cd18抗体预处理来抵消,但这种治疗并不影响肝脏VO2和DO2的改变。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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