Antenatal betamethasone-dose-effects on fetal rat lung morphology and surfactant

Lohninger, Alfred; Böck, Peter; Salzer, H; Sevelda, P.; Lohninger, A

doi:10.1515/jpme.1994.22.4.319

Cited by 8 publications

(6 citation statements)

References 24 publications

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“…It seems plausible that the effects of the lower betamethasone dose on the foetal lung is mediated by this factor, since higher concentrations of glucocorticoid are required to produce an effect on type II cells (27,28). This is supported by previous findings that in glucocorticoid-treated animals differentiation of foetal lung tissue was advanced in regions with broad epithelial-mesenchymal contact, i. e. in the terminal branches of the pseudoglandular outgrowths in the subpleural regions (29).…”

Section: Resultsmentioning

confidence: 66%

Effects of Prenatal Treatment with Betamethasone,L-Carnitine, or Betamethasone-L-Carnitine Combinations on the Phosphatidylcholine Content and Composition of the Foetal and Maternal Rat Lung

Lohninger¹,

Krieglsteiner²,

Hajos³

et al. 1996

CCLM

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Pregnant rats received 0.10 or 0.20 mg/kg body weight betamethasone, or 100 mg/kg body weight L-carnitine, or L-carnitine 100 mg/kg plus betamethasone 0.05 or 0.10 mg/kg body weight, or saline (controls) for three days before delivery of foetuses at day 19 of gestation. Dose-related effects on the dipalmitoyl phosphatidylcholine content and the phosphatidylcholine species composition of foetal and maternal lungs were determined. Betamethasone (0.10 and 0.20 mg/kg) or L-carnitine (100 mg/kg) significantly increased (p < 0.05) the dipalmitoyl phosphatidylcholine content in the foetal lungs, while only small changes were found in relative terms. Combinations of betamethasone (0.05 or 0.10 mg/kg) with L-carnitine (100 mg/kg) also significantly increased the dipalmitoyl phosphatidylcholine content of the foetal lungs above control values (p < 0.01) and above the values achieved with betamethasone alone (p < 0.05). In the maternal lungs a significant increase of the dipalmitoyl phosphatidylcholine content above the control values was only found after treatment with betamethasone-carnitine combinations, whereas compared with the foetal lung the relative increase of dipalmitoyl phosphatidylcholine as a fraction of total phosphatidylcholine was more pronounced after betamethasone treatment. The gas Chromatographie method used separates two monoenoic phosphatidylcholine species with 32 carbon atoms in the acyl residues. These two phosphatidylcholine species showed striking differences between adult and foetal lungs. Palmitoleyl palmitoyl phosphatidylcholine predominates in the maternal lung, whereas palmitoyl palmitoleyl phosphatidylcholine is the major monoenoic phosphatidylcholine species with 32 carbon atoms in the foetal lung. These two species were not affected in maternal or foetal lung by betamethasone or L-carnitine treatment. In contrast, after treatment with betamethasone-carnitine combinations, a significant increase of the fraction of palmitoyl palmitoleyl phosphatidylcholine was found in foetal but not in the maternal lung. The results of the present study demonstrate that maternal glucocorticoid and carnitine treatment affects the maternal as well as the foetal lung but with different effects on the dipalmitoyl phosphatidylcholine content and phosphatidylcholine species composition.

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Section: Resultsmentioning

confidence: 66%

Effects of Prenatal Treatment with Betamethasone,L-Carnitine, or Betamethasone-L-Carnitine Combinations on the Phosphatidylcholine Content and Composition of the Foetal and Maternal Rat Lung

Lohninger¹,

Krieglsteiner²,

Hajos³

et al. 1996

CCLM

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“…The rabbits were sequentially assigned to receive either intramuscular betamethasone (n=4) or saline (n=4). The dose of betamethasone in pregnant women is 12.5 mg once daily for 2 days; and average weight of pregnant women is about 60 kg 23. On this basis, we calculated a dose of 0.2 mg/kg (12.5/60= 0.2) daily for 2 days in pregnant rabbits.…”

Section: Methodsmentioning

confidence: 99%

Effect of Prenatal Glucocorticoids on Cerebral Vasculature of the Developing Brain

Vinukonda

Dummula

Malik

et al. 2010

Stroke

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Background and Purpose-Prenatal glucocorticoids prevent germinal matrix hemorrhage in premature infants. The underlying mechanism, however, is elusive. Germinal matrix is enriched with angiogenic vessels exhibiting paucity of pericytes and glial fibrillary acidic protein-positive astrocyte end feet. Therefore, we asked whether glucocorticoid treatment would suppress angiogenesis and enhance periendothelial coverage by pericytes and glial fibrillary acidic protein-positive end feet in the germinal matrix microvasculature. Methods-We treated pregnant rabbits with intramuscular betamethasone and delivered pups prematurely by cesarean section at E29 (termϭ32 days). Endothelial turnover, vascular density, pericyte coverage, glial fibrillary acidic protein-positive end feet, cell death, and growth factors orchestrating angiogenesis, including vascular endothelial growth factor, angiopoietins, transforming growth factor-␤, and platelet-derived growth factor-B, were compared between betamethasone-treated and untreated pups. Similar comparisons were done between autopsy materials from premature infants exposed and unexposed to prenatal glucocorticoids. Results-Antenatal glucocorticoid treatment reduced endothelial proliferation, vascular density, and vascular endothelial growth factor expression in the germinal matrix of both rabbits and humans. The pericyte coverage was greater in glucocorticoid-treated rabbit pups and human infants than in controls, but not the glial fibrillary acidic protein-positive end feet coverage. Transforming growth factor-␤, but not angiopoietins and platelet-derived growth factor-B, were elevated in glucocorticoid-treated rabbit pups compared with controls. Betamethasone treatment induced apoptosis, neuronal degeneration, and gliosis in rabbit pups. However, there was no evidence of increased cell death in glucocorticoid-exposed human infants. Conclusions-Prenatal glucocorticoid suppresses vascular endothelial growth factor and elevates transforming growth factor-␤ levels, which results in angiogenic inhibition, trimming of neovasculature, and enhanced pericyte coverage. These changes contribute to stabilizing the germinal matrix vasculature, thereby reducing its propensity to hemorrhage. Prenatal glucocorticoid exposure does not induce neural cell death in humans, unlike rabbits. (Stroke. 2010;41:1766-1773.)

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“…The dose of betamethasone administered to the pregnant rabbit was based on a) the recommended prenatal dose (12.5 mg/daily, 2 doses) for pregnant women in preterm labor to prevent respiratory distress syndrome in premature infants and b) the dose used in animal models by previous investigators (Lohninger et al, 1994, Mutafoglu et al, 2004). For these experiments, pups were sacrificed at 2 h (0d) or 72 h (3d) postnatal age.…”

Section: Methodsmentioning

confidence: 99%

Prenatal betamethasone does not affect glutamatergic or GABAergic neurogenesis in preterm newborns

et al. 2014

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Prenatal glucocorticoids (GCs) are routinely used for pregnant women in preterm labor to prevent respiratory distress syndrome and intraventricular hemorrhage in premature infants. However, the effect of antenatal GCs on neurogenesis in preterm neonates remains elusive. Herein, we hypothesized that prenatal GCs might suppress both glutamatergic and GABAergic neurogenesis in preterm rabbits and that this treatment would induce distinct changes in the expression of transcription factors regulating these developmental events. To test our hypotheses, we treated pregnant rabbits with betamethasone at E27 and E28, delivered the pups at E29 (term=32d), and assessed neurogenesis at birth and postnatal day 3. We quantified radial glia (Sox2+) and intermediate progenitor cells (Tbr2+) in the dorsal cortical subventricular zone to assess glutamatergic neuronal progenitors, and counted Nkx2.1+ and Dlx2+ cells in the ganglionic eminence to evaluate GABAergic neurogenesis. In addition, we assayed transcription factors regulating neurogenesis. We found that prenatal GCs did not affect the densities of radial glia and intermediate progenitors of glutamatergic or GABAergic neurons. The number of GABA+ interneurons in the ganglionic eminence was similar between the prenatal GC treated pups compared to untreated controls. Moreover, the mRNA expression of transcription factors, including Pax6, Ngn1/2, Emx1/2, Insm1, Dlx1, Nkx2.1, and Gsh2, were comparable between the two groups. However, there was a transient elevation in Mash1 protein in betamethasone treated pups relative to controls at birth. This data suggests that prenatal GC treatment does not significantly impact the balance of glutamatergic and GABAergic neurogenesis in premature infants.

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Antenatal betamethasone-dose-effects on fetal rat lung morphology and surfactant

Cited by 8 publications

References 24 publications

Effects of Prenatal Treatment with Betamethasone,L-Carnitine, or Betamethasone-L-Carnitine Combinations on the Phosphatidylcholine Content and Composition of the Foetal and Maternal Rat Lung

Effects of Prenatal Treatment with Betamethasone,L-Carnitine, or Betamethasone-L-Carnitine Combinations on the Phosphatidylcholine Content and Composition of the Foetal and Maternal Rat Lung

Effect of Prenatal Glucocorticoids on Cerebral Vasculature of the Developing Brain

Prenatal betamethasone does not affect glutamatergic or GABAergic neurogenesis in preterm newborns

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