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Dehydroepiandrosterone, an endogenous immune modulator, after traumatic shock
M J Schurr1, T C Fabian, M A Croce
1Department of Surgery, Presley Regional Trauma Center, University of Tennessee Health Science Center, Memphis 38163, USA.
Shock (Augusta, Ga.)
|January 1, 1997
Summary
Dehydroepiandrosterone (DHEA) did not protect against sepsis in a large-animal trauma model. Despite DHEA administration, endotoxin challenge still caused severe systemic inflammation and organ failure, indicating a lack of protective effect.
Area of Science:
- Immunology
- Endocrinology
- Critical Care Medicine
Background:
- Dehydroepiandrosterone (DHEA) modulates the immune system and reduces mortality in rodent models of endotoxin exposure.
- Clinical relevance and efficacy of DHEA in large-animal models of trauma and sepsis remain uninvestigated.
Purpose of the Study:
- To evaluate the protective effects of DHEA in a large-animal model of resuscitated trauma and delayed endotoxin challenge.
- To assess DHEA's impact on the systemic inflammatory response and organ failure following lipopolysaccharide (LPS) administration.
Main Methods:
- Anesthetized pigs underwent trauma and hemorrhage, followed by resuscitation with DHEA or vehicle.
- Animals received multiple DHEA doses over 72 hours before a lipopolysaccharide (LPS) challenge.
- Physiological parameters and DHEA levels were monitored throughout the experiment.
Main Results:
- Lipopolysaccharide (LPS) administration suppressed endogenous DHEA levels.
- Exogenous DHEA administration did not prevent the development of septic symptoms, hyperdynamic state, or pulmonary failure post-LPS.
- Treated animals showed higher DHEA levels post-LPS, but this did not correlate with improved outcomes.
Conclusions:
- DHEA levels are suppressed by LPS in this trauma-sepsis model.
- Exogenous DHEA administration failed to mitigate the systemic inflammatory response and pulmonary failure induced by LPS in resuscitated trauma pigs.