Myers D A, Robertshaw D, Nathanielsz P W
Laboratory for Pregnancy and Newborn Research, New York State College of Veterinary Medicine, Cornell University, Ithaca.
Endocrinology. 1990 Nov;127(5):2328-35. doi: 10.1210/endo-127-5-2328.
The effect of bilateral splanchnic nerve (SPLX) section in fetal sheep [116-121 days gestational age (dGA)] on subsequent adrenocortical function was investigated. Fetal cortisol release was stimulated by 1) ACTH-(1-24) administration (100 ng/min for 15 min) at 126-129 and at 132-135 dGA, and 2) nitroprusside-induced hypotension (50% reduction in fetal arterial blood pressure for 10 min) at 129-132 and 136-139 dGA. No differences were observed between SPLX and control fetuses (CONT) in basal arterial plasma concentrations of cortisol from 126-141 dGA. A significant effect of fetal age on basal cortisol was observed in both SPLX and CONT fetuses from 126-141 dGA. A significant (P less than or equal to 0.05) increase in fetal arterial concentrations of cortisol was achieved by ACTH-(1-24) infusion in SPLX and CONT and did not differ between groups at either 126-129 or 132-135 dGA. Hypotension induced a significant increase in fetal plasma cortisol concentrations in SPLX and CONT fetuses (P less than or equal to 0.05). SPLX fetuses secreted significantly less cortisol in response to hypotension than CONT fetuses at both 129-132 and 136-139 dGA (P less than 0.05). Fetal arterial plasma concentrations of immunoreactive ACTH in response to hypotension were not different between CONT and SPLX fetuses. We estimated the half-life of endogenous fetal plasma cortisol after both hypotension and infusion of ACTH-(1-24). There were no differences between either method of inducing cortisol release on the endogenous cortisol half-life, nor were any differences in cortisol half-life observed between SPLX and CONT. At 136-139 dGA the adrenomedullary response to hypotension was abolished in SPLX, confirming completeness of denervation. In conclusion, the splanchnic nerves do not appear to be involved in the normal increase in basal fetal plasma cortisol observed in late gestation in fetal sheep. However, splanchnic nerve modulation of secretion of cortisol in response to stress may be involved in the increased fetal adrenal sensitivity to stress observed late in gestation.
研究了双侧内脏神经（SPLX）切断术对胎羊[妊娠116 - 121天（dGA）]随后肾上腺皮质功能的影响。在126 - 129天和132 - 135天胎龄时，通过以下方式刺激胎儿皮质醇释放：1）给予促肾上腺皮质激素（ACTH）-(1 - 24)（100 ng/分钟，持续15分钟）；在129 - 132天和136 - 139天胎龄时，2）硝普钠诱导低血压（胎儿动脉血压降低50%，持续10分钟）。在126 - 141天胎龄期间，SPLX组胎儿与对照组（CONT）胎儿的基础动脉血浆皮质醇浓度未观察到差异。在126 - 141天胎龄期间，SPLX组和CONT组胎儿的基础皮质醇水平均受胎龄显著影响。在126 - 129天或132 - 135天胎龄时，通过ACTH-(1 - 24)输注，两组胎儿动脉皮质醇浓度均显著（P≤0.05）升高，且两组间无差异。低血压诱导SPLX组和CONT组胎儿血浆皮质醇浓度显著升高（P≤0.05）。在129 - 132天和136 - 139天胎龄时，SPLX组胎儿对低血压反应分泌的皮质醇显著少于CONT组胎儿（P＜0.05）。CONT组和SPLX组胎儿对低血压反应时的动脉血浆免疫反应性ACTH浓度无差异。我们估计了低血压和输注ACTH-(1 - 24)后内源性胎儿血浆皮质醇的半衰期。两种诱导皮质醇释放的方法对内源性皮质醇半衰期均无差异，SPLX组和CONT组之间的皮质醇半衰期也无差异。在136 - 139天胎龄时，SPLX组胎儿对低血压的肾上腺髓质反应消失，证实去神经支配完全。总之，内脏神经似乎不参与胎羊妊娠后期观察到的胎儿基础血浆皮质醇的正常升高。然而，内脏神经对应激时皮质醇分泌的调节可能与妊娠后期观察到的胎儿肾上腺对应激敏感性增加有关。
