Terminal complement complex in porcine septic shock with substantial capillary leak syndrome

Introduction

In septic shock with capillary leak syndrome (CLS), it has been suggested that hemodilution, and capillary leakage of protein may account in part for reduced levels of complement proteins observed in sepsis . Aim of this study was to determine complement activation by terminal complement complex (TCC) in septic shock under the conditions of substantial CLS.

Methods

Ten anaesthetised, and multi-catheterised pigs (20.6 ± 1.3 kg) were investigated over a period of 8 h. Sepsis was induced by fecal peritonitis. Animals were infused using 6% hydroxyethyl starch 200/0.5 to maintain a CVP of 12 mmHg. In kidneys biopsies TCC deposition was detected immunohistologically. Plasma levels of TCC were measured in a double antibody EIA using the neoepitope-specific MoAb aE11 as catching antibody. Albumin escape rate (AER; tc 99 m-labeled albumin), serum protein (S-Protein), and hematocrit (Hct) were determined. After verifying normal data distribution (skewness < 1.5) Student's t-test was performed by rank-ordered stepwise testing. Data are mean ± SD.

Results

Septic animals showed marked renal deposition of TCC. Other results, see Table.

Table

Conclusion

Although plasma levels of TCC declined over study period, in septic animals marked renal depositions of TCC indicated complement activation. Since AER increased and serum protein levels decreased, capillary loss of TCC into organ tissue may explain our findings in part. We conclude that in septic shock with substantial CLS plasma levels of TCC may not reflect degree of complement activation.