Borg T, Gerdin B, Hällgren R, Warolin O, Modig J
Acta Anaesthesiol Scand. 1984 Apr;28(2):158-65. doi: 10.1111/j.1399-6576.1984.tb02034.x.
Pulmonary leucostasis induced by complement activation has been considered an important pathogenic factor in adult respiratory distress syndrome (ARDS). To determine whether complement activation per se could evoke pulmonary dysfunction similar to ARDS, pigs were repeatedly infused with complement-activated plasma (CAP). Complement activation was produced by incubation of plasma with zymosan. Three groups of animals were investigated. Control animals received non-activated plasma. Nine animals (Group II) were given four infusions of CAP at a rate of 7 ml X min-1, and another nine animals (Group III) received two CAP infusions at a rate of 7 ml X min-1 followed by two at a rate of 14 ml X min-1. In the control animals there were no changes in gas exchange or haemodynamic variables and the leucocyte counts gradually increased. Infusion of CAP resulted in transient peripheral leucopenia and a dose-rate-dependent reversible increase in pulmonary vascular resistance in all animals. In one animal of Group II and in six of Group III there was a significant infusion-related decrease in Pao2 due to increased venous admixture. These animals were characterized by an enhanced pulmonary vascular tone before the start of the first CAP infusion. They also displayed a more pronounced pulmonary vascular response to infusion of CAP. The changes in gas exchange variables and pulmonary haemodynamics showed no relation to the degree of leucopenia or decrease in platelet count. The increased venous admixture was caused by "dry" ventilation/perfusion mismatching and not by oedema. These results suggest that additional factors besides complement activation and pulmonary leucostasis are required for the development of increased microvascular permeability and the pulmonary oedema characterizing ARDS.
补体激活所致的肺白细胞淤滞被认为是成人呼吸窘迫综合征（ARDS）的一个重要致病因素。为了确定补体激活本身是否能引发类似于ARDS的肺功能障碍，对猪反复输注补体激活血浆（CAP）。通过将血浆与酵母聚糖孵育产生补体激活。研究了三组动物。对照组动物输注未激活的血浆。9只动物（第二组）以7ml×min-1的速率接受4次CAP输注，另外9只动物（第三组）以7ml×min-1的速率接受2次CAP输注，随后以14ml×min-1的速率接受2次输注。对照组动物的气体交换或血流动力学变量无变化，白细胞计数逐渐增加。输注CAP导致所有动物出现短暂的外周血白细胞减少以及肺血管阻力呈剂量率依赖性可逆增加。在第二组的1只动物和第三组的6只动物中，由于静脉血掺杂增加，Pao2出现了与输注相关的显著下降。这些动物的特点是在首次输注CAP之前肺血管张力增强。它们对输注CAP也表现出更明显的肺血管反应。气体交换变量和肺血流动力学的变化与白细胞减少程度或血小板计数降低无关。静脉血掺杂增加是由“干性”通气/血流不匹配引起的，而非水肿所致。这些结果表明，除了补体激活和肺白细胞淤滞外，ARDS特征性的微血管通透性增加和肺水肿的发生还需要其他因素。
