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Complement-dependent hemodynamic and hematologic changes in the rabbit
Insights
Cobra factor (CoF) injection causes rapid, reversible drops in blood pressure and platelets, dependent on complement C3. Histamine H2-receptor blockade prevents these CoF-induced effects.
Area of Science:
- Immunology
- Pharmacology
- Physiology
Background:
- Cobra factor (CoF) is an anticomplementary protein that activates the complement system.
- The complement system plays a crucial role in immune responses and inflammation.
- Endotoxins from bacteria can trigger significant physiological responses.
Purpose of the Study:
- To investigate the effects of cobra factor (CoF) on blood pressure and platelets in rabbits.
- To determine the role of complement component C3 in CoF-induced changes.
- To compare the effects of CoF with those of *Serratia marcescens* endotoxin.
Main Methods:
- Intravenous injection of CoF and *S. marcescens* endotoxin in rabbits.
- Measurement of mean arterial blood pressure and circulating platelet counts.
- Utilizing rabbits genetically deficient in complement component C6.
- Employing C3 depletion strategies.
- Administering the histamine H2-receptor antagonist burimamide.
Main Results:
- CoF injection caused rapid, reversible decreases in blood pressure and platelets, dependent on complement C3.
- These CoF-induced effects were blocked by burimamide, suggesting a histamine-mediated mechanism.
- *S. marcescens* endotoxin induced acute, C3-dependent changes in blood pressure and platelets.
- C3 depletion did not affect the prolonged hypotensive and platelet-lowering effects or lethality of endotoxin.
Conclusions:
- Complement C3 is essential for the acute hypotensive and thrombocytopenic effects of CoF.
- Histamine release, mediated via H2 receptors, is involved in the CoF-induced response.
- The acute effects of *S. marcescens* endotoxin are C3-dependent, but later responses and lethality are not.
Abstract:
The intravenous injection of the anticomplementary protein from cobra venom, cobra factor (CoF),2 induces decreases in mean arterial blood pressure and circulating platelets in rabbits. The changes are rapidly reversed. Both changes require the presence of C3 and occur in rabbits genetically deficient in the sixth component of complement. The hypotensive effects of CoF were blocked by the histamine H2-receptor antagonist burimamide. An acute C3-dependent change in blood pressure and circulating platelets also was demonstrated following the intravenous injection of S. marcescens endotoxin. However, abrogation of these acute changes by C3 depletion did not alter the extent of a second, prolonged fall in blood pressure and platelets induced by S. marcescens endotoxin occurring after 60--90 min. C3 depletion also did not alter the lethal effects of the S. marcescens endotoxin.