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. 1996;19(2):129–134. doi: 10.1007/BF02805226

Complement inhibition by soluble complement receptor type 1 fails to moderate cerulein-induced pancreatitis in the rat

Martin R Weiser 1,2, Simon A L Gibbs 1,2, Francis D Moore 1,2, Herbert B Hechtman 1,2,✉
PMCID: PMC7101985  PMID: 8723555

Summary

Conclusion

Cerulein-induced pancreatitis in rats associated with remote liver and lung dysfunction. Soluble complement receptor 1 (sCR1) does not reduce the local or remote injury. Thus complement activation does not moderate cerulein-induced pancreatitis or the associated liver and lung injury.

Background

The local and remote injury of pancreatitis resembles other inflammatory events that are mediated by complement. This study examines the effect of complement inhibition with sCR1 in cerulein-induced pancreatitis in rats.

Methods

Thirteen Sprague-Dawley rats received five hourly subcutaneous doses of cerulein (100 μg initially, then 50 μg/kg). Six of these animals received hourly iv sCR1 (15 mg/kg, a proven complement-inhibiting dose in rats) and the other seven received iv saline. In parallel, 12 additional rats received hourly sc and iv saline.

Results

Compared to saline controls, rats receiving cerulein showed increased pancreatic wet-to-dry ratio (3.25∶8.52) hematocrit (40 to 47%), ascites volume (2.1 to 6.1 mL), serum amylase (1680 to 10,700 U/L), and ascites amylase (32,200 to 167,000 U/L) (allp<0.05). None of these parameters were modified by treatment with sCR1. Serum SGPT, which increased from 33.4 to 46.6 U/L in cerulein-infused rats, showed a trend toward reduction to 38.8 U/L in rats treated with sCR1. Cerulein-treated rats also had increased lung myeloperoxidase (0.069 to 0.097 U/g) and lung permeability, as assessed by alveolar lavage to serum ratio of labeled albumen (0.041∶0.121) (bothp<0.05). Neither were changed by sCR1 treatment.

Key Words: Acute Pancreatitis, cerulein, complement activation, soluble complement receptor type-1, remote pulmonary injury, neutrophils, inflammation, rodents

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