Pekna M, Nilsson L, Nilsson-Ekdahl K, Nilsson U R, Nilsson B
Department of Clinical Immunology and Transfusion Medicine, University Hospital, Uppsala, Sweden.
Clin Exp Immunol. 1993 Mar;91(3):404-9. doi: 10.1111/j.1365-2249.1993.tb05916.x.
Earlier we have shown that iC3 is generated at the blood-gas interface in vitro and that the generation of this molecule is independent of complement activation and the composition of the gas. In order to investigate whether iC3 is also generated during cardiopulmonary bypass where blood comes into contact with oxygen bubbles, two bubble oxygenators were incubated at 37 degrees C with human heparinized blood. A continuous increase in the level of iC3 was shown in the oxygen-perfused bubble oxygenator (up to 100 nmol/l after 180 min) in contrast to the unbubbled control. Similarly, in plasma drawn from patients undergoing cardiopulmonary bypass using either bubble or membrane oxygenators, the levels of iC3 were shown to increase continuously during the operation. Furthermore, this form of C3 was found to be susceptible to cleavage by factor I. The formation of iC3 at the blood-gas interface in vivo could be a mechanism by which gas bubbles induce clinical manifestations associated with complement activation, e.g. during cardiopulmonary bypass, adult respiratory distress syndrome and decompression sickness.
我们之前已经表明,iC3在体外的血气界面生成,且该分子的生成与补体激活及气体组成无关。为了研究在血液与氧气泡接触的体外循环过程中是否也会生成iC3,将两个鼓泡式氧合器于37℃与人肝素化血液一起孵育。与未鼓泡的对照组相比,在氧灌注的鼓泡式氧合器中iC3水平持续升高(180分钟后高达100 nmol/L)。同样,在使用鼓泡式或膜式氧合器进行体外循环的患者所抽取的血浆中,iC3水平在手术过程中持续升高。此外,发现这种形式的C3易被I因子裂解。体内血气界面处iC3的形成可能是气泡诱导与补体激活相关的临床表现的一种机制,例如在体外循环、成人呼吸窘迫综合征和减压病期间。