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The relationship between post-burn increases in peripheral resistance and vasopressin
Burns, Including Thermal Injury
|August 1, 1986
Summary
Blocking vasopressin (V-1 receptor) significantly reduced increased peripheral resistance after severe burns in dogs. This suggests vasopressin contributes to vasoconstriction following thermal injury.
Area of Science:
- Physiology
- Pharmacology
- Burn Medicine
Background:
- Thermal injury, such as severe burns, triggers physiological responses that can impact cardiovascular function.
- Vasopressin is a hormone known to cause vasoconstriction and its role in burn shock is not fully understood.
Purpose of the Study:
- To investigate the role of vasopressin in the increased peripheral resistance observed after a severe burn.
- To evaluate the efficacy of a vasopressin V-1 receptor antagonist in mitigating burn-induced cardiovascular changes.
Main Methods:
- An experimental model using dogs with a 15% total body surface flame burn was employed.
- Animals received either a vasopressin V-1 receptor antagonist (d(CH2)5Tyr(Me)AVP) or no treatment prior to burn.
- Peripheral resistance, cardiac output, mean arterial blood pressure, and plasma vasopressin levels were measured post-burn.
Main Results:
- Administration of the vasopressin antagonist significantly reduced the increase in peripheral resistance compared to controls.
- Peripheral resistance increased from baseline to 128.0 +/- 20.3 units immediately post-burn in untreated animals.
- Plasma vasopressin levels significantly increased post-burn, correlating with elevated peripheral resistance.
Conclusions:
- Severe thermal injury leads to a significant release of vasopressin.
- The increased peripheral resistance following burns is, in part, mediated by the vasoconstrictor action of released vasopressin.
- Blocking V-1 receptors may be a therapeutic strategy to manage burn-induced cardiovascular dysfunction.
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