Abstract
Background: Exposure to alcohol during fetal life has been associated with poor neurodevelopmental outcome; episodic (binge) exposure is considered to particularly harmful. However, the mechanisms leading to altered neurological development remain to be fully elucidated.
Objective: The aim of these on-going studies is to identify mechanisms of altered fetal brain development following repeated, “binge” exposure to ethanol (EtOH).
Methods: EtOH (1g/kg of maternal weight) was administered to 7 twin-bearing, chronically catheterized pregnant ewes over 1 hour on 3 consecutive days at 0.7 of gestation. We measured fetal and maternal blood alcohol concentrations (BAC), as well as fetal blood gases, glucose and lactate concentrations, mean arterial pressure (MAP) and heart rate. Fetal brains were subsequently analysed histologically. Data were analysed by ANOVA and are presented as mean ±SEM.
Results: BAC in the mother and fetus reached maximal values of 0.11±0.01 g/dL (∼20 mmol/L) 1h after the start of EtOH infusions. Following the EtOH infusions, fetal pH significantly increased to reach a maximum at 4h (7.37±0.004) and was still elevated at 6h relative to pre-EtOH values of 7.34±0.003. Fetal PaCO2 decreased significantly from pre-EtOH (48.7±0.7 mmHg) to reach minimum values at 4h (43.2±0.9 mmHg) and it remained decreased at 6h. Fetal PaO2 increased significantly after EtOH, relative to pre-EtOH values (17.8±0.7 mmHg) to reach peak values at 2h (20.5±0.3 mmHg) and 4h (20.4±0.6 mmHg) and it remained elevated at 6h. Fetal blood cortisol levels did not change. No significant changes were observed in maternal blood gases or glucose levels; however maternal blood lactate significantly increased from pre-EtOH values (0.5±0.07 mmol/L) to reach a maximum value at 2h (1.7±0.14 mmol/L) and it remained elevated at 6h. Histological analysis revealed white matter gliosis in 3 of 8 EtOH treated fetuses studied, white matter damage in the cerebellum of 2 of 8 EtOH fetuses and no hippocampal damage in any fetus.
Conclusions: Alterations in fetal blood gases and glucose levels following EtOH are suggestive of reduced metabolic activity by the fetus. Fetuses were not hypoxemic; therefore gliosis noted in some fetal brains induced by EtOH are most likely to be a result of mechanisms other than cerebral hypoxia.
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Dalitz, P., Rees, S., Henschke, P. et al. 109 Episodic Alcohol Consumption During Pregnancy: Mechanisms of Fetal Brain Injury. Pediatr Res 56, 482 (2004). https://doi.org/10.1203/00006450-200409000-00132
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DOI: https://doi.org/10.1203/00006450-200409000-00132
