Terminal complement complex in septic shock with capillary leakage: marker of complement activation?

Terminal complement complex in septic shock with capillary leakage: marker of complement activation?
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DOI:
10.1017/s0265021505000931
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发表时间:
2005-07-01
影响因子:
3.6
通讯作者:
Marx, G
Marx, G
中科院分区:
医学2区
文献类型:
--
作者:
Schuerholz, T;Leuwer, M;Marx, G

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背景和目的:本研究的目的是评价终末补体复合物(C5 b-9)血浆水平作为脓毒性休克伴毛细血管渗漏综合征补体激活标志物的价值。研究方法:在一项前瞻性动物研究中,对10头禁食、麻醉、机械通气和多次插管的猪(20.6 +/- 1.3 kg)进行了8小时的研究。通过粪便腹膜炎(1 g kg(-1)体重粪便,n = 5)诱导脓毒症,并与对照组(n = 5)进行比较。动物接受6%羟乙基淀粉200/0.5,以维持12 mmHg的中心静脉压。为了量化毛细血管渗漏综合征,使用Tc-99 m标记的人血清白蛋白测量白蛋白逃逸率。在双抗体免疫测定中测量末端补体复合物的血浆水平(新表位特异性MoAb aE 11作为捕获抗体)。对肾标本进行免疫组织化学研究,以检测终末补体复合物沉积。结果:脓毒症组蛋白逃逸率(+52%)高于对照组(+3%,P < 0.05)。在研究期间,两组的终末补体复合物血浆水平均降低。在脓毒症动物中,这一发现伴随着肾标本中末端补体复合物的显著沉积(P < 0.05)。结论:我们发现补体系统的激活证明了肾脏标本中的末端补体复合物的显着沉积,而其血浆水平下降,在败血症和对照动物的研究期间。这些结果表明,在伴有毛细血管渗漏综合征的脓毒性休克中,血浆末端补体复合物水平可能不是补体激活的可靠标志物。
Background and objective: The aim of this study was to evaluate the value of terminal complement complex (C5b-9) plasma levels as a marker for complement activation in septic shock with concomitant capillary leak syndrome. Methods: In a prospective animal study 10 fasted, anaesthetized, mechanically ventilated and multi-catheterized pigs (20.6 +/- 1.3 kg) were investigated over a period of 8 h. Sepsis was induced by faecal peritonitis (1 g kg(-1) body weight faeces, n = 5) and compared to controls (n = 5). The animals received 6% hydroxyethyl starch 200/0.5 to maintain a central venous pressure of 12 mmHg. To quantify capillary leak syndrome, albumin escape rate was measured using Tc-99m-labelled human serum albumin. Plasma levels of terminal complement complex were measured in a double antibody immunoassay (neoepitope-specific MoAb aE11 as catching antibody). Immunohistological studies of renal specimens were performed to detect terminal complement complex deposition. Results: Albumen escape rate increased in septic animals (+52%) compared to controls (+ 3%, P < 0.05). Plasma levels of terminal complement complex decreased during the study period in both groups. In septic animals this finding was accompanied by a significant deposition of terminal complement complex in renal specimens (P < 0.05). Conclusion: We found an activation of the complement system proven by marked deposition of terminal complement complex in renal specimen, while its plasma levels decreased during the study period in septic and control animals. These results suggest that in septic shock with capillary leak syndrome plasma level of terminal complement complex may not be a reliable marker of complement activation.