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Peripheral circulatory alterations in canine anaphylactic shock.
The American Journal of Physiology
|November 1, 1986
Summary
Anaphylactic shock causes decreased cardiac output and arterial pressure. Key factors include increased venous return resistance and systemic pressure-volume curve shifts, not plasma volume loss.
Area of Science:
- Cardiovascular Physiology
- Immunology
- Shock Pathophysiology
Background:
- Anaphylactic shock is characterized by a significant drop in cardiac output and arterial pressure.
- The precise peripheral circulatory mechanisms driving these changes remain incompletely understood.
Purpose of the Study:
- To investigate the roles of peripheral circulatory variables in the hemodynamic alterations observed during anaphylactic shock.
- To differentiate between acute plasma volume loss and other factors contributing to reduced arterial pressure.
Main Methods:
- Utilized a right heart bypass model in six dogs, administering Ascaris suum antigen to induce anaphylaxis.
- Measured cardiac output, arterial pressure, resistance to venous return, mean systemic pressure, and vascular compliance.
- Assessed plasma volume changes using protein oncotic pressure and hematocrit in intact and splenectomized dogs.
Main Results:
- Intravenous antigen administration led to a 53% decrease in cardiac output and a 58% decrease in arterial pressure.
- Resistance to venous return significantly increased, while vascular compliance remained unchanged.
- Estimates indicated small increases in plasma volume during the hypotensive phase, contradicting acute volume loss.
Conclusions:
- The primary drivers of anaphylactic shock's circulatory effects are increased resistance to venous return and a rightward shift in the systemic pressure-volume curve.
- Acute plasma volume loss is not the main mechanism responsible for the observed hypotension in anaphylaxis.