Casanueva F F, Burguera B, Muruais C, Dieguez C
Department of Medicine, Hospital General Galicia, Santiago de Compostela, Spain.
J Clin Endocrinol Metab. 1990 Jan;70(1):234-7. doi: 10.1210/jcem-70-1-234.
It is widely accepted that chronic administration of corticoids in man inhibits the GH response to all of the stimuli tested so far. To study the action of corticoids administered acutely, several dexamethasone challenge tests were performed, after which GH levels were measured for 7 h. In eight volunteers, administration of 4 mg dexamethasone (Dex), iv, induced a clear-cut GH release compared with saline administration. The secretion followed an unusual pattern; basal GH levels (1.5 +/- 0.1 micrograms/L) started rising 2 h after Dex injection, reaching a peak of 17.5 +/- 4.4 micrograms/L after 3 or 3.5 h. Peak levels were maintained until 5 h post-Dex and decreased thereafter. Similar data were obtained when Dex was administered to five volunteers at the dose of 8 mg, orally, with a 30-min delay of the GH peak (19.6 +/- 7.9 micrograms/L). To study whether there was a cholinergic input responsible for the Dex action, another group of eight volunteers underwent three Dex tests (4 mg, iv) on three occasions, followed 90 min later by the administration of placebo (control), atropine (0.5 mg, iv), or pyridostigmine (120 mg, orally). The Dex-induced GH peak (20.8 +/- 5.2 micrograms/L) was not significantly increased by pyridostigmine (cholinergic agonist) treatment (24.2 +/- 4.0 micrograms/L). The blockade of muscarinic receptors by atropine induced a delay in the Dex-induced secretory peak, which appeared at 5 h. However, the Dex-atropine GH peak (14.9 +/- 4.1 micrograms/L) was not different from the Dex-placebo one. In conclusion, Dex alone is able to induce a clear-cut GH secretion in man. The stimulus followed a peculiar time pattern, with peaks levels attained 3 h after either iv or oral administration.
人们普遍认为，长期给予人体皮质类固醇会抑制生长激素（GH）对迄今为止所测试的所有刺激的反应。为了研究急性给予皮质类固醇的作用，进行了几次地塞米松激发试验，之后测量7小时内的GH水平。在8名志愿者中，静脉注射4毫克地塞米松（Dex）与注射生理盐水相比，引起了明显的GH释放。其分泌遵循一种不寻常的模式；基础GH水平（1.5±0.1微克/升）在Dex注射后2小时开始上升，在3或3.5小时后达到峰值17.5±4.4微克/升。峰值水平一直维持到Dex注射后5小时，此后下降。当以8毫克的剂量口服给予5名志愿者Dex时，获得了类似的数据，GH峰值延迟30分钟出现（19.6±7.9微克/升）。为了研究是否存在负责Dex作用的胆碱能输入，另一组8名志愿者分三次进行了三次Dex试验（4毫克，静脉注射），90分钟后分别给予安慰剂（对照）、阿托品（0.5毫克，静脉注射）或吡啶斯的明（120毫克，口服）。吡啶斯的明（胆碱能激动剂）治疗（24.2±4.0微克/升）并未使Dex诱导的GH峰值（20.8±5.2微克/升）显著增加。阿托品对毒蕈碱受体的阻断导致Dex诱导的分泌峰值延迟，该峰值出现在5小时。然而，Dex-阿托品的GH峰值（14.9±4.1微克/升）与Dex-安慰剂的峰值并无差异。总之，单独使用Dex能够在人体中诱导明显的GH分泌。这种刺激遵循一种特殊的时间模式，静脉注射或口服给药后3小时达到峰值水平。
