Antenatal Dexamethasone after Asphyxia Increases Neural Injury in Preterm Fetal SheepReportar como inadecuado

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Background and Purpose

Maternal glucocorticoid treatment for threatened premature delivery dramatically improves neonatal survival and short-term morbidity; however, its effects on neurodevelopmental outcome are variable. We investigated the effect of maternal glucocorticoid exposure after acute asphyxia on injury in the preterm brain.


Chronically instrumented singleton fetal sheep at 0.7 of gestation received asphyxia induced by complete umbilical cord occlusion for 25 minutes. 15 minutes after release of occlusion, ewes received a 3 ml i.m. injection of either dexamethasone 12 mg, n = 10 or saline n = 10. Sheep were killed after 7 days recovery; survival of neurons in the hippocampus and basal ganglia, and oligodendrocytes in periventricular white matter were assessed using an unbiased stereological approach.


Maternal dexamethasone after asphyxia was associated with more severe loss of neurons in the hippocampus CA3 regions, 290±76 vs 484±98 neurons-mm2, mean±SEM, P<0.05 and basal ganglia putamen, 538±112 vs 814±34 neurons-mm2, P<0.05 compared to asphyxia-saline, and with greater loss of both total 913±77 vs 1201±75-mm2, P<0.05 and immature-mature myelinating oligodendrocytes in periventricular white matter 66±8 vs 114±12-mm2, P<0.05, vs sham controls 165±10-mm2, P<0.001. This was associated with transient hyperglycemia peak 3.5±0.2 vs. 1.4±0.2 mmol-L at 6 h, P<0.05 and reduced suppression of EEG power in the first 24 h after occlusion maximum −1.5±1.2 dB vs. −5.0±1.4 dB in saline controls, P<0.01, but later onset and fewer overt seizures.


In preterm fetal sheep, exposure to maternal dexamethasone during recovery from asphyxia exacerbated brain damage.

Autor: Miriam E. Koome, Joanne O. Davidson, Paul P. Drury, Sam Mathai, Lindsea C. Booth, Alistair Jan Gunn, Laura Bennet



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