Seelig R, Lankisch P G, Koop H, Winckler K, Kaboth U, Seelig H P
Res Exp Med (Berl). 1978 Dec 27;174(1):57-65. doi: 10.1007/BF01851939.
The role of the complement system was studied in Na-taurocholate pancreatitis in rats. Complement activity (CH 50) was determined at various times in the course of pancreatitis. Immediately after induction of acute pancreatitis, serum complement activity declined and massive C 3 deposits could be detected in the vicinity of acinar necroses and necrobioses. After a phase of recovery three to six hours postoperatively a second complement consumption occurred. Lethality rate increased as serum complement activity fell below 50% of preoperative values. The degree of C 3 deposition increased up to six hours. Decline of serum complement activity and deposition within the pancreas seemed to be correlated with histologically demonstrable tissue lesion. The first decline of complement activity in serum is thought to be caused by liberation of complement activating substances within the pancreas due to the detergent action of Na-taurocholate itself. The second decline, however, may be due to the liberation of complement activating and/or destroying enzymes into the blood stream.
研究了补体系统在大鼠牛磺胆酸钠诱导的胰腺炎中的作用。在胰腺炎病程的不同时间测定补体活性（CH 50）。急性胰腺炎诱导后，血清补体活性立即下降，在腺泡坏死和渐进性坏死附近可检测到大量C3沉积。术后三至六小时的恢复阶段后，发生了第二次补体消耗。当血清补体活性降至术前值的50%以下时，致死率增加。C3沉积程度在六小时内增加。血清补体活性的下降和胰腺内的沉积似乎与组织学上可证实的组织损伤相关。血清中补体活性的首次下降被认为是由于牛磺胆酸钠本身的去污剂作用导致胰腺内补体激活物质的释放。然而，第二次下降可能是由于补体激活和/或破坏酶释放到血流中。
