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