Plasma beta-endorphin immunoreactivity in dogs during anesthesia, surgery, Escherichia coli sepsis, and naloxone therapy.

To improve understanding of the role of endorphins in septic shock, we examined the effects of anesthesia, splenectomy, live Escherichia coli infusion, and treatment with naloxone, respectively, on plasma beta-endorphin immunoreactivity (beta-EI) and plasma cortisol in dogs. Baseline levels of plasma beta-EI and cortisol were established in awake dogs. Pentobarbital anesthesia alone did not affect plasma beta-EI, but splenectomy was followed by a significant (P less than 0.001) rise in both plasma beta-EI and cortisol. Infusion of saline over a 3-hour period following splenectomy induced no further increase in plasma beta-EI, but infusion of live E. coli in splenectomized dogs caused a further rise in plasma beta-EI (P less than 0.02). Following induction of septic shock in a separate group of splenectomized animals, treatment with naloxone (3 mg/kg bolus and 2 mg/kg/hr infusion) did not alter the rise in plasma beta-EI. These results confirm release of beta-endorphin during septic shock and further implicate the hypothalamic-pituitary-adrenal axis in its pathophysiology. Based on the finding that naloxone did not affect the dynamics of plasma beta-EI, mechanisms are postulated to explain the therapeutic value of this drug in septic shock.