Berghorn K A, Albrecht E D, Pepe G J
Department of Physiology, Eastern Virginia Medical School, Norfolk 23501.
Endocrinology. 1991 Sep;129(3):1424-8. doi: 10.1210/endo-129-3-1424.
The present study was designed to determine whether the baboon fetal pituitary at midgestation was responsive in utero to a bolus injection of CRH. On day 100 of gestation (term = day 184), baboons were anesthetized with halothane/nitrous oxide, the fetus was exteriorized, and a cannula was inserted into a fetal carotid artery. Five minutes later (experimental time zero), a fetal carotid blood sample was obtained, and saline (0.5 ml) with (n = 6) or without (n = 3) ovine CRH (100 ng estimated to equal 500 ng/kg BW) was then infused via the fetal carotid over a 3-min period. Fetal blood samples were taken 5, 15, 30, 45, and 60 min post-CRH/saline treatment and assayed for ACTH. Mean (+/- SE) pretreatment fetal plasma ACTH concentrations were similar in animals that subsequently received saline (26 +/- 3 pg/ml) or CRH (29 +/- 6 pg/ml). Fetal plasma ACTH remained constant after the infusion of saline. In contrast, CRH increased (P less than 0.05) fetal plasma ACTH within 5 min in six of six baboons to a value (58 +/- 12 pg/ml) that exceeded (P less than 0.05) the zero time value and the respective mean value (27 +/- 5 pg/ml) in saline-treated fetuses. Fetal plasma ACTH concentrations continued to rise in four of six baboons 15 min after CRH injection to a level (68 +/- 15 pg/ml) which exceeded that in saline controls (27 +/- 2 pg/ml). In fetuses treated with CRH, overall mean fetal plasma ACTH concentrations from 0-60 min increased at a rate (1.47 pg/min) greater (P less than 0.05) than that in fetuses injected with saline (0.07 pg/min). In contrast to the effects of intracarotid CRH injection, fetal plasma ACTH was not increased after the infusion of 100 ng CRH into a fetal antecubital vein of three additional animals. Collectively, these findings indicate that intracarotid injection of a bolus of CRH into the baboon fetus rapidly increased fetal plasma ACTH concentrations. Moreover, the site of action of CRH was presumably the fetal pituitary. Therefore, we suggest that the baboon fetal hypothalamic-pituitary axis at midgestation has the capacity to secrete ACTH in response to a challenge of CRH.
本研究旨在确定妊娠中期的狒狒胎儿垂体在子宫内是否对促肾上腺皮质激素释放激素（CRH）的单次注射有反应。在妊娠第100天（足月为第184天），用氟烷/一氧化二氮麻醉狒狒，将胎儿取出，将套管插入胎儿颈动脉。5分钟后（实验时间零点），采集胎儿颈动脉血样，然后在3分钟内通过胎儿颈动脉注入含（n = 6）或不含（n = 3）羊CRH（估计100 ng相当于500 ng/kg体重）的生理盐水（0.5 ml）。在CRH/生理盐水处理后5、15、30、45和60分钟采集胎儿血样并检测促肾上腺皮质激素（ACTH）。随后接受生理盐水（26±3 pg/ml）或CRH（29±6 pg/ml）处理的动物，预处理前胎儿血浆ACTH浓度相似。注入生理盐水后，胎儿血浆ACTH保持恒定。相比之下，在6只狒狒中有6只在注入CRH后5分钟内胎儿血浆ACTH升高（P<0.05），达到（58±12 pg/ml）的值，超过（P<0.05）零时的值以及生理盐水处理胎儿的相应平均值（27±5 pg/ml）。在6只狒狒中有4只在注入CRH后15分钟胎儿血浆ACTH浓度继续升高至（68±15 pg/ml）的水平，超过生理盐水对照组（27±2 pg/ml）。在用CRH处理的胎儿中，0至60分钟的总体平均胎儿血浆ACTH浓度以（1.47 pg/分钟）的速率升高，高于（P<0.05）注入生理盐水的胎儿（0.07 pg/分钟）。与颈动脉内注射CRH的效果相反，在另外3只动物的胎儿肘前静脉注入100 ng CRH后，胎儿血浆ACTH并未升高。总体而言，这些发现表明向狒狒胎儿颈动脉内注射一剂CRH可迅速升高胎儿血浆ACTH浓度。此外，CRH的作用部位可能是胎儿垂体。因此，我们认为妊娠中期的狒狒胎儿下丘脑 - 垂体轴有能力在CRH刺激下分泌ACTH。
