title: Plasma beta-endorphin immunoreactivity in dogs during anesthesia, surgery, Escherichia coli sepsis, and naloxone therapy.
abstract: 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.
mesh_terms: D000758:Anesthesia; D000818:Animals; D004285:Dogs; D004723:Endorphins / Q000097:blood* / Q000276:immunology; D004926:Escherichia coli; D006854:Hydrocortisone / Q000097:blood; D009270:Naloxone / Q000494:pharmacology / Q000627:therapeutic use; D011183:Postoperative Complications; D011863:Radioimmunoassay; D018805:Sepsis / Q000150:complications; D012772:Shock, Septic / Q000097:blood* / Q000209:etiology; D013156:Splenectomy; D001615:beta-Endorphin
chemical_list: D004723:Endorphins; D009270:Naloxone; D001615:beta-Endorphin; D006854:Hydrocortisone