Endorphins in septic shock: hemodynamic and endocrine effects of an opiate receptor antagonist and agonist
F. N. Gahhos, R. C. Chiu, E. J. Hinchey and G. K. Richards
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.