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Related Experiment Videos

Complement inhibition with soluble complement receptor type 1 in cardiopulmonary bypass

A M Gillinov1, P A DeValeria, J A Winkelstein

  • 1Department of Cardiac Surgery, Johns Hopkins Medical Institutions, Baltimore, Maryland.

The Annals of Thoracic Surgery
|March 1, 1993
PubMed
Summary

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Complement activation contributes to lung injury after cardiopulmonary bypass (CPB). Soluble human complement receptor type 1 (sCR1) effectively inhibited complement, reducing lung injury in a porcine CPB model.

Area of Science:

  • Cardiovascular Surgery
  • Immunology
  • Pulmonary Medicine

Background:

  • Complement activation is known to occur during cardiopulmonary bypass (CPB).
  • The specific role of complement activation in causing postperfusion organ injury, particularly lung injury, remains unproven.

Purpose of the Study:

  • To investigate the contribution of complement activation to pulmonary injury during CPB.
  • To assess the efficacy of soluble human complement receptor type 1 (sCR1) in mitigating CPB-induced lung injury.

Main Methods:

  • Utilized a porcine model of hypothermic (28°C) CPB for 2 hours.
  • Administered sCR1, a complement inhibitor, to the treatment group (12 mg/kg IV).
  • Measured complement activity (total hemolytic, C3, C5) and pulmonary parameters (vascular resistance, alveolar-arterial gradient) post-CPB.

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Main Results:

  • sCR1 effectively inhibited both classic and alternative complement pathways in pigs.
  • Control piglets showed significant reductions in complement activity during CPB.
  • sCR1-treated piglets exhibited a significantly lower increase in pulmonary vascular resistance post-CPB compared to controls.
  • No significant differences were observed in alveolar-arterial gradients or myeloperoxidase levels, suggesting specific effects on vascular resistance.

Conclusions:

  • Complement activation plays a direct pathogenic role in lung injury following cardiopulmonary bypass.
  • Inhibition of complement activation with sCR1 can attenuate CPB-induced pulmonary vascular dysfunction.