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Formation of prostanoids during intravascular complement activation in the rabbit
British Journal of Pharmacology
|February 1, 1985
Summary
Cobra venom factor (CVF) activates complement, increasing plasma levels of prostacyclin and thromboxane B2. These prostanoid elevations correlate with hypotension and thrombocytopenia, suggesting a role in endotoxin shock.
Area of Science:
- Biochemistry
- Immunology
- Pharmacology
Background:
- Prostaglandins, such as prostacyclin and thromboxane B2, are key mediators of inflammatory and haemodynamic responses.
- The complement system plays a critical role in innate immunity and can be activated by various triggers, including endotoxins.
Purpose of the Study:
- To investigate the effect of complement activation on plasma levels of specific prostanoids.
- To explore the relationship between complement activation, prostanoid formation, and haemodynamic changes.
Main Methods:
- Radioimmunoassay (RIA) was used to quantify plasma concentrations of 6-oxo-prostaglandin F1 alpha and thromboxane B2.
- Arterial blood samples were collected before and after intravenous administration of cobra venom factor (CVF).
Main Results:
- CVF administration led to dose-dependent and reversible increases in plasma 6-oxo-PGF1 alpha and TXB2 levels.
- The temporal patterns of prostanoid elevation mirrored those of arterial hypotension and thrombocytopenia.
Conclusions:
- Complement activation by CVF stimulates the formation of arachidonic acid metabolites.
- These complement-dependent prostanoids are implicated in the haemodynamic and haematological alterations observed in endotoxin shock.