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Division of Perinatal Medicine in the Departments of 1 Obstetrics and Gynecology and 2 Pediatrics; 3 Pediatric Heart Lung Center, University of Colorado Health Sciences Center; and 4 Department of Pathology, Childrens Hospital, Denver, Colorado 80262
Heat exposure early in
ovine pregnancy results in placental insufficiency and intrauterine
growth restriction (PI-IUGR). We hypothesized that heat exposure in
this model disrupts placental structure and reduces placental
endothelial nitric oxide synthase (eNOS) protein expression. We
measured eNOS protein content and performed immunohistochemistry for
eNOS in placentas from thermoneutral (TN) and hyperthermic (HT) animals
killed at midgestation (90 days). Placental histomorphometry was
compared between groups. Compared with the TN controls, the HT group
showed reduced delivery weights (457 ± 49 vs. 631 ± 21 g; P < 0.05) and a trend for reduced placentome
weights (288 ± 61 vs. 554 ± 122 g; P = 0.09). Cotyledon eNOS protein content was reduced by 50% in the HT
group (P < 0.03). eNOS localized similarly to the
vascular endothelium and binucleated cells (BNCs) within the
trophoblast of both experimental groups. HT cotyledons showed a
reduction in the ratio of fetal to maternal stromal tissue (1.36 ± 0.36 vs. 3.59 ± 1.2; P
0.03). We conclude that
eNOS protein expression is reduced in this model of PI-IUGR and that
eNOS localizes to both vascular endothelium and the BNC. We speculate
that disruption of normal vascular development and BNC eNOS production
and function leads to abnormal placental vascular tone and blood flow
in this model of PI-IUGR.
endothelial nitric oxide synthase; hyperthermia; placenta; binucleate cell; intrauterine growth restriction
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