Florian Rakers1, Sabine Bischoff2, Rene Schiffner3, Michelle Haase3, Sven Rupprecht3, Michael Kiehntopf4, W Nikolaus Kühn-Velten5, Harald Schubert2, Otto W Witte6, Mark J Nijland7, Peter W Nathanielsz7, Matthias Schwab3. 1. Hans Berger Department of Neurology, Jena University Hospital, Jena, Germany. Electronic address: florian.rakers@med.uni-jena.de. 2. Institute of Laboratory Animal Sciences and Welfare, Jena University Hospital, Jena, Germany. 3. Hans Berger Department of Neurology, Jena University Hospital, Jena, Germany. 4. Institute of Clinical Chemistry and Laboratory Medicine, Jena University Hospital, Jena, Germany. 5. Medical Laboratory Bremen, Bremen, Germany. 6. Hans Berger Department of Neurology, Jena University Hospital, Jena, Germany; Center for Sepsis Control and Care, Jena University Hospital, Jena, Germany. 7. Center for Pregnancy and Newborn Research, Department of Obstetrics and Gynecology, University of Texas, San Antonio, School of Medicine, San Antonio, TX.
Abstract
OBJECTIVE: We sought to evaluate whether in addition to cortisol, catecholamines also transfer psychosocial stress indirectly to the fetus by decreasing uterine blood flow (UBF) and increasing fetal anaerobic metabolism and stress hormones. STUDY DESIGN: Seven pregnant sheep chronically instrumented with uterine ultrasound flow probes and catheters at 0.77 gestation underwent 2 hours of psychosocial stress by isolation. We used adrenergic blockade with labetalol to examine whether decreased UBF is catecholamine mediated and to determine to what extent stress transfer from mother to fetus is catecholamine dependent. RESULTS: Stress induced transient increases in maternal cortisol and norepinephrine (NE). Maximum fetal plasma cortisol concentrations were 8.1 ± 2.1% of those in the mother suggesting its maternal origin. In parallel to the maternal NE increase, UBF decreased by maximum 22% for 30 minutes (P < .05). Fetal NE remained elevated for >2 hours accompanied by a prolonged blood pressure increase (P < .05). Fetuses developed a delayed and prolonged shift toward anaerobic metabolism in the presence of an unaltered oxygen supply. Adrenergic blockade prevented the stress-induced UBF decrease and, consequently, the fetal NE and blood pressure increase and the shift toward anaerobic metabolism. CONCLUSION: We conclude that catecholamine-induced decrease of UBF is a mechanism of maternal-fetal stress transfer. It may explain the influence of maternal stress on fetal development and on programming of adverse health outcomes in later life especially during early pregnancy when fetal glucocorticoid receptor expression is limited.
OBJECTIVE: We sought to evaluate whether in addition to cortisol, catecholamines also transfer psychosocial stress indirectly to the fetus by decreasing uterine blood flow (UBF) and increasing fetal anaerobic metabolism and stress hormones. STUDY DESIGN: Seven pregnant sheep chronically instrumented with uterine ultrasound flow probes and catheters at 0.77 gestation underwent 2 hours of psychosocial stress by isolation. We used adrenergic blockade with labetalol to examine whether decreased UBF is catecholamine mediated and to determine to what extent stress transfer from mother to fetus is catecholamine dependent. RESULTS: Stress induced transient increases in maternal cortisol and norepinephrine (NE). Maximum fetal plasma cortisol concentrations were 8.1 ± 2.1% of those in the mother suggesting its maternal origin. In parallel to the maternal NE increase, UBF decreased by maximum 22% for 30 minutes (P < .05). Fetal NE remained elevated for >2 hours accompanied by a prolonged blood pressure increase (P < .05). Fetuses developed a delayed and prolonged shift toward anaerobic metabolism in the presence of an unaltered oxygen supply. Adrenergic blockade prevented the stress-induced UBF decrease and, consequently, the fetal NE and blood pressure increase and the shift toward anaerobic metabolism. CONCLUSION: We conclude that catecholamine-induced decrease of UBF is a mechanism of maternal-fetal stress transfer. It may explain the influence of maternal stress on fetal development and on programming of adverse health outcomes in later life especially during early pregnancy when fetal glucocorticoid receptor expression is limited.
Authors: Joana Krämer; Rui Kang; Laura M Grimm; Luisa De Cola; Pierre Picchetti; Frank Biedermann Journal: Chem Rev Date: 2022-01-07 Impact factor: 60.622
Authors: Brendan D Ostlund; Kristen Olavson; Mindy A Brown; Nila Shakiba; Celine Saenz; Sheila E Crowell; Elisabeth Conradt Journal: Dev Psychobiol Date: 2021-05-30 Impact factor: 3.038
Authors: Mary C Wallingford; Ciara Benson; Nicholas W Chavkin; Michael T Chin; Martin G Frasch Journal: Front Physiol Date: 2018-08-07 Impact factor: 4.755
Authors: Brendan D Ostlund; Koraly E Pérez-Edgar; Shannon Shisler; Sarah Terrell; Stephanie Godleski; Pamela Schuetze; Rina D Eiden Journal: Dev Psychopathol Date: 2021-10-15
Authors: A B Janssen; D A Kertes; G I McNamara; E C Braithwaite; H D J Creeth; V I Glover; R M John Journal: J Neuroendocrinol Date: 2016-08 Impact factor: 3.627