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目的：证明一定条件下，旁路活化补体可使ＫＣ吞噬杀菌功能失常。方法：观测定量培养的ＫＣ在ＺＡＨＳ作用下吞噬杀菌及分泌杀菌致炎物质功能的动态水平；观察大鼠肠系膜注射ＺＡＨＳ后肝组织的病理改变；以抗人Ｃ３、Ｃ５血清中和的ＺＡＨＳ进行反证。结果：①ＺＡＨＳ处理组，ＫＣ的ＰＩ和ＩＣＢＡ以及胞内Ｏ－２水平先升后降，胞内ＡＣＰ水平只降无升；ＩＣＢＡ与Ｏ－２和ＡＣＰ的水平均显著相关；各指标至６ｈ降至最低；②阻断组Ｏ－２、ＡＣＰ、ＩＣＢＡ在６ｈ水平保持在正常对照组的９７％、８３％和７９％，显著高于ＺＡＨＳ处理组；③肠系膜静脉注射ＺＡＨＳ１２ｈ后，大鼠肝组织轻度变性，部分ＫＣ线粒体受损，与ＫＣ相邻肝细胞出现凋亡改变，阻断组肝组织无明显病变。结论：ＺＡＨＳ中过量的Ｃ３、Ｃ５碎片持续作用能使ＫＣ吞噬杀菌功能下降，对肝组织结构亦有一定间接破坏作用。这些都有利于并发感染发生
PURPOSE: To demonstrate that under certain conditions, KC phagocytosis can be dysfunctional by activating the complement bypasses. Methods: The kinetic levels of phagocytotic bactericidal and bactericidal and inflammatory substances under the action of ZAHS were observed. The pathological changes of liver tissue were observed after the mesenteric injection of ZAHS in rats. . Results: ① The levels of PI and ICBA and intracellular O-2 in ZAHS treatment group increased first and then decreased, while the intracellular ACP level decreased only but not increased; the levels of ICBA and O-2 and ACP were significantly correlated; (2) The levels of O-2, ACP and ICBA in the blocking group kept at 97%, 83% and 79% of the normal control group at 6h, which were significantly higher than those in the ZAHS treatment group. (3) After the mesenteric vein was injected with ZAHS for 12h, the rat liver tissue Mild degeneration, some KC mitochondrial damage, and KC adjacent hepatocytes apoptosis, blocking group no significant pathological changes in liver tissue. Conclusion: The continuous action of excess C3 and C5 fragments in ZAHS can decrease the phagocytosis and bactericidal activity of KC, and also indirectly destroy the structure of liver. These are conducive to the occurrence of concurrent infections