La Marca-Ghaemmaghami Pearl, Dainese Sara M, La Marca Roberto, Zimmermann Roland, Ehlert Ulrike
From the Department of Psychology, Clinical Psychology and Psychotherapy (P.L.M.-G., S.M.D., R.L.M., U.E.), University of Zurich, Zurich, Switzerland; and the Department of Obstetrics (R.Z.), University Hospital Zurich, Zurich, Switzerland.
Psychosom Med. 2015 Jan;77(1):41-9. doi: 10.1097/PSY.0000000000000130.
The maternal autonomic nervous system (ANS) has received little attention in the investigation of biological mechanisms linking prenatal stress to fetal cortisol (F) excess. In vitro, norepinephrine and epinephrine inhibit placental 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), which protects the fetus from F overexposure by inactivating it to cortisone (E). Here, we investigated the acute ANS stress response to an amniocentesis and its association with amniotic fluid F, E, and E/(E + F) as a marker of fetoplacental 11β-HSD2 activity.
An aliquot of amniotic fluid was obtained from 34 healthy, second-trimester pregnant women undergoing amniocentesis. Repeated assessment of mood states served to examine the psychological stress response to amniocentesis. Saliva samples were collected to measure stress-induced changes in salivary α-amylase concentrations in response to amniocentesis. Cardiac parameters were measured continuously.
Undergoing amniocentesis induced significant psychological and autonomic alterations. Low-frequency (LF)/high-frequency (HF) baseline, suggested to reflect sympathovagal balance, was negatively correlated with amniotic E/(E + F) (r=-0.53, p = .002) and positively with F (r = 0.62, p < .001). In contrast, a stronger acute LF/HF response was positively associated with E/(E + F) (r = 0.44, p = .012) and negatively with F (r=-0.40, p = .025).
These findings suggest that the maternal ANS is involved in the regulation of the fetoplacental barrier to stress. Allostatic processes may have been initiated to counterbalance acute stress effects. In contrast, higher LF/HF baseline values, possibly indicative of chronic stress exposure, may have inhibited 11β-HSD2 activity in the fetoplacental unit. These results parallel animal findings of up-regulated placental 11β-HSD2 in response to acute stress but impairment under chronic stress.
在探究产前应激与胎儿皮质醇（F）过量之间生物学机制的研究中，母体自主神经系统（ANS）很少受到关注。在体外，去甲肾上腺素和肾上腺素会抑制2型胎盘11β-羟类固醇脱氢酶（11β-HSD2），该酶通过将F转化为可的松（E）来保护胎儿免受F过度暴露的影响。在此，我们研究了羊膜穿刺术引起的急性ANS应激反应及其与羊水F、E以及作为胎儿胎盘11β-HSD2活性标志物的E/（E + F）之间的关联。
从34名接受羊膜穿刺术的健康孕中期孕妇中获取一份羊水样本。通过对情绪状态的反复评估来检查对羊膜穿刺术的心理应激反应。收集唾液样本以测量羊膜穿刺术引起的唾液α-淀粉酶浓度的应激诱导变化。持续测量心脏参数。
进行羊膜穿刺术会引起显著的心理和自主神经改变。低频（LF）/高频（HF）基线被认为反映交感迷走神经平衡，它与羊水E/（E + F）呈负相关（r = -0.53，p = 0.002），与F呈正相关（r = 0.62，p < 0.001）。相反，更强的急性LF/HF反应与E/（E + F）呈正相关（r = 0.44，p = 0.012），与F呈负相关（r = -0.40，p = 0.025）。
这些发现表明母体ANS参与了胎儿胎盘对应激的屏障调节。可能已经启动了应变调节过程来平衡急性应激效应。相比之下，较高的LF/HF基线值可能表明长期暴露于应激，这可能抑制了胎儿胎盘单位中的11β-HSD2活性。这些结果与动物研究结果一致，即胎盘11β-HSD2在急性应激下上调，但在慢性应激下受损。
