Dubey A K, Plant T M
Biol Reprod. 1985 Sep;33(2):423-31. doi: 10.1095/biolreprod33.2.423.
Four orchidectomized rhesus monkeys (3-3.5 yr of age) were treated for 62 days with daily i.m. injections of hydrocortisone acetate (HCA) at a dose of 10-20 mg/(kg BW X day), and blood samples were obtained daily or every other day before, during, and after treatment. Hydrocortisone acetate injections resulted in a progressive rise in mean plasma cortisol from basal concentrations of 17-35 micrograms/100 ml prior to initiation of steroid treatment to approximately 150 micrograms/100 ml 5 wk later. When serum cortisol concentrations reached 100 micrograms/100 ml, 3-4 wk after the initiation of HCA treatment, circulating luteinizing hormone (LH) and follicle-stimulating hormone (FSH) began to decline, reaching nondetectable concentrations 35 days later. Withdrawal of HCA resulted in a return in plasma cortisol concentrations to pretreatment control levels, which was associated with a complete restoration of gonadotropin secretion. In 2 animals, administration of an intermittent i.v. infusion of gonadotropin-releasing hormone (GnRH) (0.1 micrograms/min for 3 min once every hour), which appears to stimulate the gonadotropes in a physiologic manner, reversed the cortisol-induced inhibition of gonadotropin secretion, restoring circulating LH and FSH concentrations to within 80-100% of control. These results suggest that, in the rhesus monkey, the major site of the inhibitory action of cortisol on gonadotropin release resides at a suprapituitary level and is mediated by interruption of hypothalamic GnRH release.
对4只去势的恒河猴（3 - 3.5岁）进行了为期62天的治疗，每天肌肉注射醋酸氢化可的松（HCA），剂量为10 - 20毫克/（千克体重×天），并在治疗前、治疗期间和治疗后每天或隔天采集血样。注射醋酸氢化可的松导致平均血浆皮质醇从类固醇治疗开始前的基础浓度17 - 35微克/100毫升逐渐升高，5周后达到约150微克/100毫升。在HCA治疗开始后3 - 4周，当血清皮质醇浓度达到100微克/100毫升时，循环中的促黄体生成素（LH）和促卵泡生成素（FSH）开始下降，35天后降至检测不到的浓度。停用HCA导致血浆皮质醇浓度恢复到治疗前的对照水平，这与促性腺激素分泌的完全恢复相关。在2只动物中，间歇性静脉输注促性腺激素释放激素（GnRH）（每小时一次，0.1微克/分钟，持续3分钟），这似乎以生理方式刺激促性腺激素细胞，逆转了皮质醇诱导的促性腺激素分泌抑制，使循环中的LH和FSH浓度恢复到对照水平的80 - 100%以内。这些结果表明，在恒河猴中，皮质醇对促性腺激素释放的抑制作用的主要部位位于垂体上水平，并且是通过下丘脑GnRH释放的中断介导的。
