University of Kentucky

Poster Title

Adding Insult to Injury: Hypoxia Following Ethanol Exposure Produces Multiplicative Damage in Vitro

Institution

University of Kentucky

Abstract

Despite knowledge of the long-term damaging effect, alcohol consumption during pregnancy continues to be a significant problem and is the leading preventable cause of mental retardation in the western world. It is not well understood why some children are more affected than others, but it is believed that a shared mechanism between alcohol withdrawal and hypoxia could have a synergistic effect. The hypothesis of this study was that prenatal alcohol exposure can reduce the ability of an organism to respond well to otherwise innocuous hypoxic challenges and therefore the combination can have far worse effects than either variable alone. The hypothesis was tested using a hippocampal slice model taken from neonatal rats as a model for the human 3rd trimester of pregnancy. Slices were exposed to either alcohol or a control solution for ten days followed by exposure to either compressed air or anaerobic gas for 15, 30, or 60 minutes. Cell damage was quantified in the CA1, CA3, and dentate gyrus of the hippocampus. The combination of ethanol withdrawal and 30 minutes of hypoxia caused multiplicative damage, while neither variable alone produced damage above control levels. These results suggest that exposure to amount of alcohol that would not cause significant damage on its own would sensitize the brain to hypoxic challenges, which could cause significant damage when in combination. This could explain the variability that is seen among the clinical population of individuals exhibiting Fetal Alcohol Spectrum Disorder. (Supported in part by NIAAA 017956 to SB).

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Adding Insult to Injury: Hypoxia Following Ethanol Exposure Produces Multiplicative Damage in Vitro

Despite knowledge of the long-term damaging effect, alcohol consumption during pregnancy continues to be a significant problem and is the leading preventable cause of mental retardation in the western world. It is not well understood why some children are more affected than others, but it is believed that a shared mechanism between alcohol withdrawal and hypoxia could have a synergistic effect. The hypothesis of this study was that prenatal alcohol exposure can reduce the ability of an organism to respond well to otherwise innocuous hypoxic challenges and therefore the combination can have far worse effects than either variable alone. The hypothesis was tested using a hippocampal slice model taken from neonatal rats as a model for the human 3rd trimester of pregnancy. Slices were exposed to either alcohol or a control solution for ten days followed by exposure to either compressed air or anaerobic gas for 15, 30, or 60 minutes. Cell damage was quantified in the CA1, CA3, and dentate gyrus of the hippocampus. The combination of ethanol withdrawal and 30 minutes of hypoxia caused multiplicative damage, while neither variable alone produced damage above control levels. These results suggest that exposure to amount of alcohol that would not cause significant damage on its own would sensitize the brain to hypoxic challenges, which could cause significant damage when in combination. This could explain the variability that is seen among the clinical population of individuals exhibiting Fetal Alcohol Spectrum Disorder. (Supported in part by NIAAA 017956 to SB).