부산대학교 도서관

To purchase or authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1113/jphysiol.2008.165944 Byline: Deborah M. Burrage (1), Lucy Braddick (1), Jane K. Cleal (1), Paula Costello (1), David E. Noakes (2), Mark A. Hanson (1), Lucy R. Green (1) Abstract: Undernourished late gestation fetuses display asymmetric growth restriction, suggestive of a redistribution of nutritional resources. The modification of fetal organ blood supply in response to acute hypoxia is well characterized, but it is not known whether similar responses occur in response to acute reductions in nutrition, or if such late gestation responses can be influenced by early gestation nutrition. In pregnant sheep, total nutrient requirements were restricted during the peri-implantation period (PI40, 40%; PI50, 50% of total, days 1-31) or in late gestation (L, 50% total, days 104-postmortem). Control animals were fed 100% nutrient requirements. Fetal organ blood flows were measured at baseline, and during acute fetal hypoglycaemia induced by maternal insulin infusion at 125 dGA. Baseline heart rate was increased in PI40 fetuses. During hypoglycaemia, an initial rise in fetal heart rate was followed by a slower fall. Fetal femoral artery blood flow decreased, and adrenal blood flow and femoral vascular resistance increased in all fetuses during hypoglycaemia. These changes were accompanied by increased fetal plasma adrenaline and cortisol, and reduced plasma insulin levels. The maximum femoral artery blood flow response to hypoglycaemia occurred earlier in PI50 and PI40 compared with control fetuses. The late gestation fetal cardiovascular response to acute hypoglycaemia was consistent with a redistribution of combined ventricular output away from the periphery and towards central organs. One element of the peripheral vascular response was modified by peri-implantation nutrient restriction, indicating that nutritional challenges early in gestation can have an enduring impact on cardiovascular control. Author Affiliation: (1)Institute of Developmental Sciences, Developmental Origins of Health and Disease Division, University of Southampton, Southampton SO16 6YD, UK (2)Department of Veterinary Reproduction, Royal Veterinary College, North Mymms, AL9 7TA, UK Article History: (Resubmitted 3 November 2008; accepted 4 December 2008; first published online 15 December 2008) Article note: Corresponding author L. R. Green: Institute of Developmental Sciences, MP887, Southampton General Hospital, Tremona Road, Southampton SO16 6YD, UK. Email: lgreen@soton.ac.uk