Naloxone without transfusion prolongs survival and enhances cardiovascular function in hypovolemic shock

The hypothesis that opiate receptors are involved in the cardiovascular pathophysiology of hypovolemic shock was tested by using the opiate receptor antagonist naloxone. Naloxone increased mean arterial pressure, cardiac output, stroke volume and left ventricular dP/dtmax in a canine hemorrhagic sho...

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Bibliographic Details
Published inThe Journal of pharmacology and experimental therapeutics Vol. 220; no. 3; pp. 621 - 624
Main Authors Gurll, N J, Reynolds, D G, Vargish, T, Lechner, R
Format Journal Article
LanguageEnglish
Published United States American Society for Pharmacology and Experimental Therapeutics 01.03.1982
Subjects
Animals
Blood Pressure - drug effects
Dogs
Dose-Response Relationship, Drug
Female
Heart Rate - drug effects
Hemodynamics - drug effects
Male
Myocardial Contraction - drug effects
Naloxone - pharmacology
Shock - drug therapy
Shock - physiopathology
Shock, Hemorrhagic - physiopathology
Time Factors
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Summary:The hypothesis that opiate receptors are involved in the cardiovascular pathophysiology of hypovolemic shock was tested by using the opiate receptor antagonist naloxone. Naloxone increased mean arterial pressure, cardiac output, stroke volume and left ventricular dP/dtmax in a canine hemorrhagic shock model. Naloxone treatment also prolonged survival time. All these responses were dose-dependent and were independent of blood reinfusion. It is concluded that endorphins activated by stress act on opiate receptors to bring about some of the cardiovascular abnormalities in hypovolemic shock.
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ISSN:0022-3565
1521-0103