Chenoweth D E, Cooper S W, Hugli T E, Stewart R W, Blackstone E H, Kirklin J W
N Engl J Med. 1981 Feb 26;304(9):497-503. doi: 10.1056/NEJM198102263040901.
We observed complement activation in 15 adults undergoing total cardiopulmonary bypass. Plasma levels of C3a were significantly elevated (P < 0.0001) at the beginning of the procedure, and they continued to increase steadily thereafter. At the end of the procedure, C3a levels were more than five times higher than preoperative levels. Plasma levels of C5a (a factor that binds avidly to neutrophils) did not change significantly during cardiopulmonary bypass. Instead, there was significant neutrophilia (P = 0.03) during bypass, and significant transpulmonary neutropenia (P = 0.0002) occurred when cardiopulmonary circulation was reestablished at partial bypass. The neutropenia is consistent with pulmonary-vascular sequestration of C5a-activated granulocytes. We also found that incubation of blood with the nylon-mesh liner of bubble oxygenators, as well as vigorous oxygenation of whole blood, promotes conversion of complement. We conclude that the complement-derived inflammatory mediators C3a and C5a produced during extracorporeal circulation may contribute to the pathogenesis of "post-pump syndromes."
我们观察了15名接受全心肺转流术的成年人的补体激活情况。手术开始时,血浆C3a水平显著升高(P < 0.0001),此后持续稳步上升。手术结束时,C3a水平比术前水平高出五倍多。血浆C5a(一种与中性粒细胞紧密结合的因子)水平在心肺转流期间无显著变化。相反,转流期间出现显著的中性粒细胞增多(P = 0.03),在部分转流恢复心肺循环时出现显著的经肺中性粒细胞减少(P = 0.0002)。中性粒细胞减少与C5a激活的粒细胞在肺血管中的滞留一致。我们还发现,血液与鼓泡式氧合器的尼龙网衬垫孵育以及全血的剧烈氧合会促进补体的转化。我们得出结论,体外循环期间产生的补体衍生炎症介质C3a和C5a可能促成“泵后综合征”的发病机制。