The effects of naloxone on central hemodynamics and myocardial metabolism in experimental propoxyphene-induced circulatory shock.
The courses of the hemodynamic and cardiometabolic effects of naloxone were evaluated in propoxyphene-induced shock in eight pentobarbital-anesthetized pigs. Circulatory shock was induced by an infusion of propoxyphene chloride 15 mg . min-1 i.v. At shock, i.e. MAP less than 60 mmHg and/or CI less than 2.0 l . min-1 . m-2, naloxone was administered at 0.75, 1.5 and 3.0 mg . kg-1 with an interval between increments of 8 min. The propoxyphene infusion of 15 mg . min-1 was continued throughout the study. Following the injection of naloxone 0.75 mg . kg-1, increases were observed (% of baseline value) in MAP (41%), i.e. deficit to baseline 59%, HR (66%), CI (67%) and SVI (108%), whereas MPAP and MPAOP were unchanged. dP/dt increased (34%). In the coronary circulation naloxone initiated the following changes: CSF increased (69%) as did MVO2 (48%) with unchanged MO2-extraction, but CVR decreased further (36%). The maximum effects of naloxone were registered 2-3 min after 0.75 mg . kg-1. Following 1.5 and 3.0 mg . kg-1, no changes in hemodynamics were observed other than those caused by progressing propoxyphene intoxication.
D000818:Animals; D011431:Dextropropoxyphene / Q000378:metabolism / Q000506:poisoning*; D006321:Heart / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects*; D009206:Myocardium / Q000378:metabolism*; D009270:Naloxone / Q000494:pharmacology*; D010424:Pentobarbital / Q000494:pharmacology; D011957:Receptors, Opioid / Q000187:drug effects; D012769:Shock / Q000139:chemically induced / Q000503:physiopathology*; D013552:Swine
D011957:Receptors, Opioid; D009270:Naloxone; D010424:Pentobarbital; D011431:Dextropropoxyphene