English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Fetal growth restriction (FGR) is a common cause of perinatal morbidity and mortality. Suboptimal uteroplacental perfusion is the most commonly identified cause of FGR, and ischemic lesions are often observed in placentas from pregnancies complicated by FGR. Ischemia followed by reperfusion is a strong stimulus to the production of the vasoconstrictor endothelin 1 (ET-1) which has been implicated in several models of FGR. We sought to investigate oxidative stress and placental morphology in a rat model of ischemia-reperfusion (I/R)-induced FGR and to evaluate the role of ET-1 in the observed pathology. Unilateral uterine I/R (30 min) was conducted, with and without simultaneous ET-1 receptor A (ET A ) antagonism, on pregnant rats at gestation day 17. Placental tissues collected 24 hours later were evaluated immunohistochemically for oxidative damage. Tissue pathology was studied using quantitative morphometry. Glycogen-rich cellular areas in the placental junctional zone exhibited only 50% intact cells (P &lt; .001) in both uterine horns following unilateral I/R, compared to controls. ET A antagonism prevented damage to the glycogen-rich cellular areas. Oxidative damage in response to I/R was prominent in the labyrinthine layer in both uterine horns and was not affected by ET A antagonism. We conclude that glycogen-rich cellular areas of the placental junctional zone are particularly vulnerable to damage from uterine I/R in the rat. Nucleic acid oxidative damage in the labyrinth is a prominent effect of uterine I/R. ET A antagonism protects placental cellular integrity during I/R challenge but does not prevent nucleic acid oxidative damage.

Endothelin Receptor A Antagonism Prevents Damage to Glycogen-Rich Placental Cells Following Uterine Ischemia–Reperfusion in the Rat