Anesthesia and Stimulation of Pituitary β-Endorphin Release in Rats

Abstract

The effects of several anesthetic drugs and artificial respiration on the release of pituitary β-endorphin-like immunoreactivity (β-END-LI) were examined in rats. Plasma β-END-LI responses to halothane and pentobarbital were similar in magnitude and duration, being maximal (2- to 3-fold) by 10 min and returning to control values by 30 min after induction. Urethane anesthesia was associated with an 8-fold increase in plasma β-END-LI throughout the 30-min treatment period. In comparison to anesthesia alone, anesthesia plus intubation with artificial respiration (standard parameters) was associated with considerably greater elevations in plasma β-END-LI (up to 30-fold). Further, intubation and artificial respiration appear to have contributed separately, and in an additive fashion, to the overall β-END-LI responses observed. As compared to halothane anesthesia alone, intubation evoked a 4-fold increase in circulating β-END-LI, whereas intubation plus ventilation was associated with a 12-fold increase. Treatment with morphine (1 or 5 mg/kg), but not pancuronium (0.3 mg/kg), attenuated the plasma β-END-LI response to mechanical ventilation, suggesting that a subconscious phenomenon, perhaps related to pain, was partially responsible for the profound release of pituitary β-END-LI associated with artificial respiration. Chromatographic analysis of the molecular forms of β-END-LI released into plasma revealed that both β-END- and β-lipotropin (β-LPH)-sized peptides were secreted under the present experimental conditions. Since the analgesic form of β-END (β-END_1-31) is cosecreted with β-LPH from the pars distalis, increases in the fraction of plasma β-END-LI corresponding to β-END in size were probably due to the release of opiate active β-END_1-31.