OPIATE RECEPTORS AND ENDORPHINS IN THE PATHO-PHYSIOLOGY OF HEMORRHAGIC-SHOCK

  • 1 January 1981
    • journal article
    • research article
    • Vol. 89  (3) , 364-369
Abstract
The hypothesis that endorphins released by stress act on opiate receptors to depress cardiovascular function during hemorrhagic shock was investigated. Anesthetized adult mongrel dogs were bled into a heparinized reservoir to achieve a mean arterial pressure (MAP) of 45 mm Hg. The reservoir was adjusted to maintain MAP for 1 h and then clamped for 1 h, after which the shed blood was reinfused. While the reservoir was clamped the animals were treated with an i.v. bolus followed by 3 h infusion of 0.9% NaCl (as control) or the specific opiate receptor antagonist naloxone at 3 dose regimens (0.5, 1 or 2 mg/kg plus 0.5, 1 or 2 mg/kg per h). Naloxone produced dose-dependent increases in MAP, cardiac output, stroke volume and left ventricular contractility. Survival at 72 h was related to the dose of naloxone used. None of 6 dogs treated at 0 mg/kg per h survived, 1 of 6 survived at 0.5 mg/kg per h, 4 of 5 at 1 ng/kg per h and 5 of 5 at 2 mg/kg per h. Since naloxone has minimal effect on cardiovascular function in nonshocked dogs; opiate receptors and perhaps endorphins are implicated in the cardiovascular pathophysiology of hemorrhagic shock.