Levin E R, Sharp B, Carlson H E
Life Sci. 1984 Oct 8;35(15):1535-45. doi: 10.1016/0024-3205(84)90351-5.
The stimulating effect of naloxone on plasma beta-endorphin immunoreactivity (beta EI) was examined in dogs. Intravenous naloxone at 5, 1, or 0.1 mg/kg caused a significant increase in beta EI while doses of 0.01 or 0.001 mg/kg had no effect. The peak plasma beta EI levels occurred at 25 mins after naloxone. The neurotransmitter and antagonists metergoline, atropine, diphenhydramine and phentolamine all failed to significantly alter basal beta EI secretion; further, they all failed to prevent the increase in beta EI resulting from naloxone administration. Dexamethasone prevented the naloxone-induced rise in beta EI. Our results suggest naloxone's effect on beta EI is not mediated through several neurotransmitter systems known to affect ACTH secretion. Additionally, beta EI secreted in response to naloxone appears to originate mainly from the anterior lobe of the pituitary.
在犬类中研究了纳洛酮对血浆β-内啡肽免疫反应性（β-EI）的刺激作用。静脉注射5、1或0.1mg/kg的纳洛酮可使β-EI显著增加，而0.01或0.001mg/kg的剂量则无作用。血浆β-EI峰值水平出现在纳洛酮给药后25分钟。神经递质及拮抗剂美替拉酮、阿托品、苯海拉明和酚妥拉明均未能显著改变基础β-EI分泌；此外，它们均未能阻止纳洛酮给药导致的β-EI增加。地塞米松可阻止纳洛酮诱导的β-EI升高。我们的结果表明，纳洛酮对β-EI的作用不是通过已知影响促肾上腺皮质激素分泌的几种神经递质系统介导的。此外，对纳洛酮产生反应而分泌的β-EI似乎主要起源于垂体前叶。
