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 in:	The Journal of pharmacology and experimental therapeutics Vol. 220; no. 3; p. 621
Main Authors:	Gurll, N J, Reynolds, D G, Vargish, T, Lechner, R
Format:	Journal Article
Language:	English
Published:	United States 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.
ISSN:	0022-3565