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Superoxide dismutase and hemodynamic changes following aortic crossclamp release
P A Casthely1, J Dluzneski, R Jones
1Department of Anesthesiology, State University of New York Health Science Center, Brooklyn, NY, USA.
Journal of Cardiothoracic Anesthesia
|August 1, 1988
Summary
Superoxide dismutase (SOD) administration significantly mitigates hypotension and maintains arterial oxygen tension after aortic crossclamp release. This free-radical scavenger protects against adverse hemodynamic changes in dogs.
Area of Science:
- Cardiovascular Physiology
- Pharmacology
- Free Radical Biology
Background:
- Aortic crossclamp release commonly causes hypotension.
- This is due to fluid sequestration and increased capillary permeability from vasoactive substances like bradykinin and free radicals.
Purpose of the Study:
- To investigate superoxide dismutase (SOD) as a pharmacological agent.
- To prevent hemodynamic alterations post-aortic crossclamping and release.
Main Methods:
- Fourteen mongrel dogs were divided into two groups.
- Group A received NaHCO3 and SOD; Group B received NaHCO3 only.
- Aorta was clamped for 60 minutes, followed by release and hemodynamic monitoring.
Main Results:
- Group A (SOD) showed improved cardiac output and stable blood pressure post-release.
- Group B experienced a significant decrease in cardiac output and arterial oxygen tension (PaO2).
- SOD administration prevented the drop in PaO2 observed in the control group.
Conclusions:
- Superoxide dismutase (SOD) effectively minimizes cardiovascular changes after aortic crossclamp release.
- SOD acts as a free-radical scavenger, preserving hemodynamic stability.
- This study highlights SOD's potential in managing post-aortic crossclamp complications.
