| All three trimester binge alcohol exposure causes fetal cerebellar purkinje cell loss in the presence of maternal hypercapnea, acidemia, and normoxemia: ovine model. | |
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MedLine Citation:
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PMID: 17511745 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: The third trimester equivalent has been identified, both in rat and sheep models, as a period of cerebellar vulnerability to alcohol-mediated injury. We wished to determine whether alcohol exposure throughout gestation results in greater injury compared with exposure limited to the third trimester equivalent. While this question has previously been addressed in the rat model, where the third trimester equivalent occurs postnatally, it has not yet been addressed in an animal model where all 3 trimester equivalents occur prenatally, as in the ovine. We also wished to correlate cerebellar Purkinje cell loss to alcohol-mediated alterations in maternal arterial pH and blood gases as these responses might be important mechanistically in mediating the damage. METHODS: Three groups of pregnant sheep were used: an untreated normal control group, a saline control group, and an alcohol group (1.75 g/kg of the body weight). The alcohol exposure regimen was designed to mimic a human binge pattern; alcohol was administered intravenously on 3 consecutive days, followed by 4 days without alcohol, beginning day 4 of gestation, continuing to the end of the third trimester equivalent of human brain growth, day 132 of gestation. RESULTS: All 3 trimester alcohol-exposed fetal brains exhibited significant deficits in cerebellar volume and Purkinje cell number compared with those of control subjects. We did not detect a difference in the reduction of Purkinje cell number when comparing between all 3 trimester and third trimester alcohol exposure studies. The neuronal loss was accompanied by maternal hypercapnea, acidemia, and normoxemia. CONCLUSIONS: These findings demonstrate in an ovine model where all 3 trimester equivalent of brain growth occur in utero that the fetal cerebellar Purkinje cells are more sensitive to the timing of alcohol exposure and less so to the duration of exposure. Decreases in maternal P(a)O(2) were not detected, suggesting that maternal hypoxia does not play a role in fetal Purkinje cell loss. And finally, we conclude that alcohol-induced changes in maternal arterial pH may play a role in alcohol-mediated developmental brain injury. |
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Authors:
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Jayanth Ramadoss; Emilie R Lunde; Kevin B Piña; Wei-Jung A Chen; Timothy A Cudd |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, N.I.H., Extramural Date: 2007-05-20 |
Journal Detail:
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Title: Alcoholism, clinical and experimental research Volume: 31 ISSN: 0145-6008 ISO Abbreviation: Alcohol. Clin. Exp. Res. Publication Date: 2007 Jul |
Date Detail:
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Created Date: 2007-06-19 Completed Date: 2007-07-24 Revised Date: 2007-12-03 |
Medline Journal Info:
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Nlm Unique ID: 7707242 Medline TA: Alcohol Clin Exp Res Country: England |
Other Details:
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Languages: eng Pagination: 1252-8 Citation Subset: IM |
Affiliation:
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Department of Veterinary Physiology and Pharmacology and Michael E DeBakey Institute, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843-4466, USA. |
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| MeSH Terms | |
Descriptor/Qualifier:
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Acidosis
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pathology Alcohol Drinking / psychology* Animals Cell Count Cerebellum / drug effects*, growth & development, pathology Disease Models, Animal* Ethanol / administration & dosage, pharmacology* Female Fetal Alcohol Syndrome / etiology* Gestational Age* Hydrogen-Ion Concentration Hypercapnia / etiology, metabolism Oxygen / blood Pregnancy Pregnancy Complications / blood, pathology, psychology* Purkinje Cells / drug effects, pathology Rats Sheep |
| Grant Support | |
ID/Acronym/Agency:
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AA10940/AA/NIAAA NIH HHS |
| Chemical | |
Reg. No./Substance:
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64-17-5/Ethanol; 7782-44-7/Oxygen |
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