The Acute Autonomic Stress Response and Amniotic Fluid Glucocorticoids in Second-Trimester Pregnant XXXX .

@entity1 @entity821 @entity27476 @entity1425 @entity701 @entity1063 @entity2342
OBJECTIVE: The maternal autonomic nervous system (ANS) has received little attention in the investigation of biological mechanisms linking prenatal stress to fetal @entity701 (F) excess. In vitro, @entity1063 and @entity1425 inhibit placental 11b-hydroxysteroid dehydrogenase type 2 (11b- @entity27476 ), which protects the fetus from F overexposure by inactivating it to @entity821 (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 11b- @entity27476 activity. METHODS: An aliquot of amniotic fluid was obtained from 34 healthy, second-trimester pregnant @entity1 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 a-amylase concentrations in response to amniocentesis. Cardiac parameters were measured continuously. RESULTS: Undergoing amniocentesis induced significant @entity2342 . 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 11b- @entity27476 activity in the fetoplacental unit. These results parallel animal findings of up-regulated placental 11b- @entity27476 in response to acute stress but impairment under chronic stress.
