Maiewski S, Muldoon S, Mueller G P
Proc Soc Exp Biol Med. 1984 Jul;176(3):268-75. doi: 10.3181/00379727-176-41870.
The effects of several anesthetic drugs and artificial respiration on the release of pituitary beta-endorphin-like immunoreactivity (beta-END-LI) were examined in rats. Plasma beta-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 beta-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 beta-END-LI (up to 30-fold). Further, intubation and artificial respiration appear to have contributed separately, and in an additive fashion, to the overall beta-END-LI responses observed. As compared to halothane anesthesia alone, intubation evoked a 4-fold increase in circulating beta-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 beta-END-LI response to mechanical ventilation, suggesting that a subconscious phenomenon, perhaps related to pain, was partially responsible for the profound release of pituitary beta-END-LI associated with artificial respiration. Chromatographic analysis of the molecular forms of beta-END-LI released into plasma revealed that both beta-END- and beta-lipotropin (beta-LPH)-sized peptides were secreted under the present experimental conditions. Since the analgesic form of beta-END (beta- END1 -31) is cosecreted with beta-LPH from the pars distalis, increases in the fraction of plasma beta-END-LI corresponding to beta-END in size were probably due to the release of opiate active beta- END1 -31.
研究了几种麻醉药物和人工呼吸对大鼠垂体β-内啡肽样免疫反应性（β-END-LI）释放的影响。血浆β-END-LI对氟烷和戊巴比妥的反应在幅度和持续时间上相似，诱导后10分钟达到最大值（增加2至3倍），30分钟后恢复到对照值。在整个30分钟的治疗期间，氨基甲酸乙酯麻醉使血浆β-END-LI增加了8倍。与单独麻醉相比，麻醉加标准参数的人工呼吸插管使血浆β-END-LI升高幅度更大（高达30倍）。此外，插管和人工呼吸似乎分别以累加的方式对观察到的总体β-END-LI反应有贡献。与单独的氟烷麻醉相比，插管使循环中的β-END-LI增加了4倍，而插管加通气则使β-END-LI增加了12倍。吗啡（1或5mg/kg）治疗可减弱血浆β-END-LI对机械通气的反应，但泮库溴铵（0.3mg/kg）则无此作用，这表明一种可能与疼痛相关的潜意识现象部分导致了与人工呼吸相关的垂体β-END-LI的大量释放。对释放到血浆中的β-END-LI分子形式进行色谱分析表明，在本实验条件下，β-内啡肽（β-END）和β-促脂素（β-LPH）大小的肽均有分泌。由于β-END的镇痛形式（β-END1 -31）与β-LPH从远侧部共同分泌，血浆中与β-END大小相对应的β-END-LI部分增加可能是由于具有阿片活性的β-END1 -31的释放所致。
