title: The acute autonomic stress response and amniotic fluid glucocorticoids in second-trimester pregnant women.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: 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.
authors.forename: Pearl
authors.initials: P
authors.lastname: La Marca-Ghaemmaghami
authors.forename: Sara M
authors.initials: SM
authors.lastname: Dainese
authors.forename: Roberto
authors.initials: R
authors.lastname: La Marca
authors.forename: Roland
authors.initials: R
authors.lastname: Zimmermann
authors.forename: Ulrike
authors.initials: U
authors.lastname: Ehlert
mesh_terms: D043209:11-beta-Hydroxysteroid Dehydrogenase Type 2 / Q000378:metabolism; D000328:Adult; D000649:Amniocentesis / Q000523:psychology*; D000653:Amniotic Fluid / Q000737:chemistry; D001341:Autonomic Nervous System / Q000378:metabolism*; D003348:Cortisone / Q000378:metabolism*; D005260:Female; D005938:Glucocorticoids; D006339:Heart Rate; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism*; D008875:Middle Aged; D011247:Pregnancy; D011262:Pregnancy Trimester, Second; D055291:Salivary alpha-Amylases / Q000378:metabolism; D013315:Stress, Psychological / Q000378:metabolism*
chemical_list: D005938:Glucocorticoids; D043209:11-beta-Hydroxysteroid Dehydrogenase Type 2; D055291:Salivary alpha-Amylases; D003348:Cortisone; D006854:Hydrocortisone