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Complement depletion and persistent hemodynamic-hematologic responses in protamine-heparin reactions.

T W Wakefield¹, G O Till, B Lindblad

¹Department of Surgery, University of Michigan Medical School, Ann Arbor 48109-0331.

The Journal of Surgical Research

|September 1, 1988

Summary

This study investigated adverse reactions to protamine-heparin reversal in complement-depleted dogs. Results indicate that complement activation is not responsible for these hemodynamic and hematologic changes.

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Area of Science:

Cardiovascular Physiology
Hematology
Immunology

Background:

Protamine sulfate is used to reverse heparin anticoagulation.
Adverse effects like hypotension and thrombocytopenia have been linked to complement activation.
This study investigates the role of complement in protamine-heparin reactions.

Purpose of the Study:

To determine if complement activation is responsible for protamine-heparin-induced hypotension, bradycardia, pulmonary artery hypertension, neutropenia, and thrombocytopenia.
To examine these phenomena in complement-depleted animals.

Main Methods:

Eight dogs were treated with cobra venom factor (CVF) to deplete complement.
Animals subsequently received heparin and protamine sulfate.
Hemodynamic parameters (BP, HR, PAS, PAD, CO) and hematologic parameters (PTC, WBC) were monitored.

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Main Results:

CVF effectively depleted complement in all dogs.
Maximal mean changes observed were: BP -43 mm Hg, HR -16, PAS +6 mm Hg, PAD +3 mm Hg, CO -27%, PTC -49%, WBC -48%.
These responses occurred despite complement depletion.

Conclusions:

Complement components C3 and C5-C9 are not influential factors in protamine-heparin-induced hemodynamic and hematologic events.
The study suggests alternative mechanisms for these adverse reactions.