Placental and fetal contraindications of dexamethasone administration to pregnant rats

Garvey, D.; Scott, Jane N.

doi:10.1007/bf01967964

Cited by 8 publications

(8 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As previously reported (Garvey and Scott, 1981), body and placenta weights of 21d DEXA-exposed fetuses were significantly lower than those of 21d controls. No gross signs of abnormal development were detected in either of the DEXA groups.…”

Section: General Fetal Developmentsupporting

confidence: 71%

“…These findings include increased fetal mortality, decreased fetal body and organ weights, cleft palate, altered placental morphology, delayed parturition, and added by this study, altered fetal adrenal corticosteroid production and ultrastructural development (Parvez et al, 1976;Ballard et al, 1977;Frank and Roberts, 1979;Garvey and Scott, 1981). The effects on the fetal adrenal glands appear to result from a direct inhibition of the hypothalamo-pituitary-adrenal axis by DEXA (D'Angelo et al, 1973;Dupouy and Coffigny, 1976).…”

Section: Discussionmentioning

confidence: 65%

See 1 more Smart Citation

Suppression of adernal cortical growth and differentiation in fetal rats exposed to dexamethasone

et al. 1983

View full text Add to dashboard Cite

The effects of maternal dexamethasone (DEXA) administration during the last days of gestation on fetal adrenal growth and differentiation were studied. Timed pregnant rats were divided into three groups: (a) 21d DEXA-3 received DEXA in drinking water (5 pg/ml) from days 18 to 21 of gestation; (b) 21d DEXAB received the same dosage of DEXA from days 15 to 21 of gestation; and (c) 21d control received tap water throughout gestation. On gestation day 21, pregnant rats were decapitated and bled into heparinized tubes; their fetuses were excised, weighed, decapitated, and bled. Fetal adrenals were prepared for electron microscopy or weighed and frozen until assayed for corticosterone. Control adrenals were also collected on day 15 of gestation and processed for electron microscopy only. Fetal adrenals were fixed in 2.5% glutaraldehyde in 0.5 M cacodylate buffer, postfixed in 2% osmium tetroxide (OsO$, dehydrated, and embedded in Epon 812. Twenty-one day (21d) fetal adrenal weights were 44% and 68% lower than control values for DEXA-3 and -6, respectively. Fetal adrenal corticosterone levels were decreased by 70% and 89% for the respective groups. These observations correlated with ultrastructural findings of decreased mitochondria1 number and size, altered orientation of the inner mitochondrial membrane, decreased lipid, and dilation of smooth endoplasmic reticulum (SER) in cortical fascicular cells of DEXA-exposed fetuses. Ultrastructural changes in the 21d DEXA fetal adrenals resembled 15d day control fetal adrenals. The results suggest suppressed adrenocortical differentiation probably due to DEXA inhibition of the steroidogenic influence of the fetal pituitary on the developing adrenal gland in DEXA-exposed fetuses.

show abstract

Section: General Fetal Developmentsupporting

confidence: 71%

Section: Discussionmentioning

confidence: 65%

Suppression of adernal cortical growth and differentiation in fetal rats exposed to dexamethasone

et al. 1983

View full text Add to dashboard Cite

show abstract

“…High affinity low capacity GRs have been identified in the placenta of various species, including man, rat, and mouse [17,35,161,162]. This would have important clinical implications, because GC-induced downregulation of the placental glucose transport system(s) may contribute to the deleterious side-effects of GC treatment during pregnancy, such as the higher incidence of growthretarded fetuses [46,[163][164][165].…”

Section: The Effects Of Glucocorticoids On Placental Glucose Transpormentioning

confidence: 99%

The Effects of Glucocorticoids on Fetal and Placental Development

Korgun¹,

Ozmen²,

Unek³

et al. 2012

Glucocorticoids - New Recognition of Our Familiar Friend

View full text Add to dashboard Cite

“…A well-known deleterious side effect of GC treatment during pregnancy is the higher incidence of growth-restricted fetuses (Reinisch et al 1978, Garvey & Scott 1981, Katz et al 1990, Edwards et al 1993, Seckl 1994 and an intrauterine programming of cardiovascular, metabolic and neuroendocrine disorders in adult life (Seckl 2004). We recently identified a downregulation of trophoblast glucose transporters by GC and hypothesised that this may contribute to the restricted fetal and placental growth observed with the GC treatment (Hahn et al 1999).…”

Section: Introductionmentioning

confidence: 99%

Differential glucocorticoid effects on proliferation and invasion of human trophoblast cell lines

Mandl

Ghaffari-Tabrizi²,

Haas³

et al. 2006

Reproduction

View full text Add to dashboard Cite

Several clinical situations require continuous glucocorticoid (GC) treatment during pregnancy. A well-known deleterious side effect of such treatment is the higher incidence of growth-restricted fetuses, for which a too shallow trophoblast invasion is presently hypothesised as the underlying cause. This study investigated whether the synthetic GC triamcinolone acetonide (TA) influences proliferation, invasion and endocrine activity of human trophoblast. BeWo and JEG-3 choriocarcinoma cell lines both express GC receptors (western blotting) and were used as models for human trophoblast. JAR devoid cells of GC receptor were used as negative control. The cells were cultured for 48 h without (control) or with 0.5, 5 and 50 mM TA. In the presence and absence of serum, proliferation was determined by cell counting and measuring the cell cycle regulating protein cyclin B1 (Western blotting); invasion was determined by a conventional Matrigel invasion assay and by measuring the secretion (ELISA) of matrix-metalloproteinases (MMP-2, MMP-9) into the culture medium; endocrine activity was assessed by measuring the levels of human chorionic gonadotropin (ELISA) into the culture medium. TA altered the number of viable and dead cells as well as cyclin B1 levels and, to a lesser extent, invasion of BeWo and JEG-3, with a strong influence of serum. BeWo and JEG-3 cells reacted differently and in most instances reverse. In the cell lines used as models of human trophoblast, TA alter some functions relevant to proliferation and invasion, and suggest that caution should be exercised when treating women with GCs during pregnancy.

show abstract

Placental and fetal contraindications of dexamethasone administration to pregnant rats

Cited by 8 publications

References 20 publications

Suppression of adernal cortical growth and differentiation in fetal rats exposed to dexamethasone

Suppression of adernal cortical growth and differentiation in fetal rats exposed to dexamethasone

The Effects of Glucocorticoids on Fetal and Placental Development

Differential glucocorticoid effects on proliferation and invasion of human trophoblast cell lines

Contact Info

Product

Resources

About