Naloxone reversal of hypovolemic shock in dogs.
The endogenous opiate ligand, beta-endorphin, is released during stress. We tested the hypothesis that endorphins may be involved in the pathophysiology of hemorrhagic shock by using the opiate receptor blocking agent, naloxone. Two groups of five anesthetized dogs were instrumented to monitor cardiovascular performance and subjected to a protocol in which they were bled into a reservoir to lower mean arterial pressure to 45 mmHg and maintained at that pressure for one hour. At that time the reservoir was clamped and on group of dogs received an intravenous bolus of naloxone (2 mg/kg) and an infusion at 2 mg/kg-hr. These dogs demonstrated a prompt increase in arterial pressure, left ventricular dp/dtmax and cardiac output. The shed blood was returned at t = 2 hr and drug infusion continued for 2 hours. The control group of dogs received saline in equivalent volume. The control dogs died within 30 minutes of clamping the reservoir while all five treated dogs survived beyond 72 hours (P less than 0.02). These data suggest the involvement of endorphins acting on opiate receptors as part of the pathophysiology in this shock model.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001810:Blood Volume; D004285:Dogs; D006339:Heart Rate / Q000187:drug effects; D007022:Hypotension / Q000188:drug therapy; D009270:Naloxone / Q000494:pharmacology*; D011957:Receptors, Opioid / Q000187:drug effects; D012769:Shock / Q000188:drug therapy*; D014655:Vascular Resistance / Q000187:drug effects
D011957:Receptors, Opioid; D009270:Naloxone