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This Article Full Text Full Text (PDF) All Versions of this Article: 92/5/933    most recent expphysiol.2007.038091v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Parnell, S. E. Articles by Cudd, T. A. Search for Related Content PubMed PubMed Citation Articles by Parnell, S. E. Articles by Cudd, T. A.

¹ Bowles Center for Alcohol Studies and Department of Cell and Developmental Biology, The University of North Carolina, Chapel Hill, NC, USA ² 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, USA ³ Department of Neuroscience and Experimental Therapeutics, College of Medicine, The Texas A&M Health Science Center, College Station, TX, USA ⁴ Division of Exercise Physiology and Center for Interdisciplinary Research in Cardiovascular Sciences, West Virginia University School of Medicine, Morgantown, WV, USA ⁵ Department of Physical Education, Exercise and Sports Sciences, East Tennessee State University, Johnson City, TN, USA

Cerebral hypoxia has been proposed as a mechanism by which prenatal ethanol exposure causes fetal alcohol spectrum disorder (FASD) in children, but no study had tested this hypothesis using a chronic exposure model that mimicks a common human exposure pattern. Pregnant sheep were exposed to ethanol, 0.75 or 1.75 g kg^–1 (to create blood ethanol concentrations of 85 and 185 mg dl^–1, respectively), or saline 3 days per week in succession (a ‘binge drinking’ model) from gestational day (GD) 109 until GD 132. Fetuses were instrumented on GD 119–120 and studied on GD 132. The 1.75 g kg^–1 dose resulted in a significant increase in fetal biventricular output (measured by radiolabelled microsphere technique) and heart rate, and a reduction of mean arterial pressure and total peripheral resistance at 1 h, the end of ethanol infusion. The arterial partial pressure of CO₂ was increased, arterial pH was decreased and arterial partial pressure of O₂ did not change. Fetal whole-brain blood flow increased by 37% compared with the control group at 1 h, resulting in increased cerebral oxygen delivery. The elevation in brain blood flow was region specific, occurring preferentially in the ethanol-sensitive cerebellum, increasing by 44% compared with the control group at 1 h. There were no changes in the lower dose group. Assessment of regional differences in the teratogenic effects of ethanol by stereological cell-counting technique showed a reduced number of cerebellar Purkinje cells in response to the 1.75 g kg^–1 dose compared with the control brains. However, no such differences in neuronal numbers were observed in the hippocampus or the olfactory bulb. We conclude that repeated exposure to moderate doses of ethanol during the third trimester alters fetal cerebral vascular function and increases blood flow in brain regions that are vulnerable to ethanol in the presence of acidaemia and hypercapnia, and in the absence of hypoxia.

(Received 6 April 2007; accepted after revision 15 May 2007; first published online 25 May 2007)
Corresponding author T. A. Cudd: Texas A&M University, Department of Veterinary Physiology and Pharmacology, Highway 60, Building VMA, Room 332, College Station, TX 77843-4466, USA. Email: tcudd{at}tamu.edu

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				C. E. Wood Maternal binge drinking and fetal neuronal damage Exp Physiol, September 1, 2007; 92(5): 821 - 821. [Full Text] [PDF]