Endorphins in septic shock: hemodynamic and endocrine effects of an opiate receptor antagonist and agonist.
The pathophysiological role of endorphins in septic shock was studied in a porcine model. Septic shock was induced by the intravenous infusion of live Escherichia coli. Naloxone hydrochloride, an opiate receptor blocker, given during profound septic shock, increased blood concentrations of glucagon and cyclic adenosine monophosphate (cAMP), while BP and cardiac output increased transiently. Heart rate and hepatic glycogen value decreased, but insulin and cortisol levels remained unchanged. In contrast, exogenous morphine injection produced further reduction of BP, increased pulmonary wedge pressure, and increased substance P, while growth hormone level and cardiac output remained unchanged. Neither hormonal nor hemodynamic changes were noted in saline controls. Thus, the endogenous opiates appear partly responsible for the hemodynamic derangements during septic shock, and naloxone is able to reverse such depression, even though the effects are transient and relatively minor when naloxone is given late in the course of septic shock. Endogenous opiates also affect the hormonal homeostasis in shock, and there are indications that this may be mediated by the adenylate cyclase-cAMP system.
D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure / Q000187:drug effects; D004723:Endorphins / Q000502:physiology*; D005260:Female; D006439:Hemodynamics / Q000187:drug effects*; D006728:Hormones / Q000097:blood*; D008297:Male; D009020:Morphine / Q000494:pharmacology*; D009270:Naloxone / Q000494:pharmacology*; D011669:Pulmonary Wedge Pressure / Q000187:drug effects; D011957:Receptors, Opioid / Q000187:drug effects; D012772:Shock, Septic / Q000097:blood / Q000503:physiopathology*; D013552:Swine
D001786:Blood Glucose; D004723:Endorphins; D006728:Hormones; D011957:Receptors, Opioid; D009270:Naloxone; D009020:Morphine