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为了实验性地消除调节促性腺激素(GTH)分泌的下丘脑-垂体功能,已有三种灵长类动物模型被广泛应用:切断垂体柄的猴、切除垂体的猴,以及经放射和电损伤的下丘脑内侧基底部被离断的猴。但根据上述外科模型的研究结果直接进行临床推断是不能被接受的。因此,作者试图通过给予一种GnRH 拮抗物取消内源 GTH 分泌,达到可逆性的“药物性垂体切除”。GnRH 拈抗物与 GnRH 受体有高度亲和力,但不具有 GnRH 所固有的生物学活性。为了减少垂体 GTH 分泌,达到接近药物性垂体切除的 GTH 低下状态,作者用了强有力的GnRH 拮抗物:[乙酰基-pCl 苯丙~1,pClD 苯丙~2D
To experimentally eliminate hypothalamic-pituitary gland function that regulates the secretion of gonadotropin (GTH), three primate models have been used: monkeys with pituitary stalk cut, pituitary-monkey removed, and radiation and electrical injury Hypothalamic medial basal ganglia were severed. However, direct clinical inference based on the results of the above surgical model can not be accepted. Therefore, the authors attempted to achieve reversible “drug-induced hypophysectomy” by abolishing endogenous GTH secretion by administering a GnRH antagonist. GnRH antagonists have high affinity for GnRH receptors but do not possess the biological activity inherent to GnRH. In order to reduce the secretion of pituitary GTH and reach the state of GTH close to drug-induced pituitary resection, the authors used potent GnRH antagonists: [acetyl-pCl phenylpropyl-1, pClD phenylpropion-2D