CQUniversity
Browse

Stress and preterm birth: Biological and vascular mechanisms affecting the feto-placental circulation and the length of gestation

Version 2 2023-01-30, 02:56
Version 1 2019-08-20, 00:00
journal contribution
posted on 2023-01-30, 02:56 authored by Afrooz Najafzadeh Abriz
Preterm birth is the leading cause of perinatal morbidity and mortality. Women experiencing high levels of stress in pregnancy are at an increased risk of preterm delivery. This review examines the biological pathways of the maternal stress response, in particular, the functioning of the maternal hypothalamic–pituitary–adrenal axis, and investigates the role of the placenta in altering this response mechanism. Furthermore, the impact of the products of hypothalamic–pituitary–adrenal axis on the blood flow resistance of the feto‐placental arteries is explained. Prior Doppler studies of maternal stress were reviewed. The study of correlations between maternal stress and resistive indices of feto‐placental arteries was common themes in these studies. Their conclusions, however, were inconsistently explained by their methodological differences and limited control for potential confounders. The biological mechanisms of stress control provide the impression that it is plausible that antenatal stress could affect the placental function and influence preterm delivery, but to date, this has not been conclusively established. If the investigation is further expanded to include measures of fetal biometry, additional blood vessels and an assessment over a longer period in gestation, subtle changes in the feto‐placental blood supply may be revealed, and a link to preterm birth is feasible.

Funding

Category 1 - Australian Competitive Grants (this includes ARC, NHMRC)

History

Volume

3

Issue

3

Start Page

95

End Page

102

Number of Pages

8

eISSN

2054-6750

ISSN

2202-8323

Publisher

Wiley

Language

en

Peer Reviewed

  • Yes

Open Access

  • No

Acceptance Date

2016-07-12

Era Eligible

  • Yes

Journal

Sonography

Usage metrics

    CQUniversity

    Exports

    RefWorks
    BibTeX
    Ref. manager
    Endnote
    DataCite
    NLM
    DC