Wollert S, Rasmussen I, Lundberg C, Gerdin B, Arvidsson D, Haglund U
Department of Surgery, University Hospital, Uppsala, Sweden.
Circ Shock. 1993 Dec;41(4):230-8.
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.
循环中的多形核白细胞（PMN）黏附于肝血管床内皮，参与了猪粪便性腹膜炎所致的肝脏氧输送（DO2）和氧消耗（VO2）的改变。22只猪被分为三组。第一组（n = 7）的动物作为对照。第二组（n = 7）和第三组（n = 8）诱导产生粪便性腹膜炎。第三组的动物用IB4进行预处理，IB4是一种抑制PMN黏附于内皮的单克隆抗CD18抗体。尽管肝脏DO2降低，但腹膜炎使第二组和第三组的肝脏VO2增加。在第一组中，实验期间循环中的PMN增加。脓毒症导致第二组循环中的PMN数量减少，而在第三组中这种作用被完全抵消，第三组中PMN数量上升至对照水平。肝脏活检中PMN浸润的髓过氧化物酶活性和形态学测定实际上与循环中的PMN计数平行。尽管粪便性腹膜炎后会出现依赖CD18的白细胞减少，且可用抗CD18抗体预处理来抵消，但这种治疗并不影响所观察到的肝脏VO2和DO2的改变。
