Blood flows and nutrient uptakes in growth-restricted pregnancies induced by overnourishing adolescent sheep

• Published in: American journal of physiology. Regulatory, integrative and comparative physiology Vol. 282; no. 4; pp. 1027 - R1036
• Main Authors: Wallace, Jacqueline M, Bourke, Deirdre A, Aitken, Raymond P, Leitch, Neil, Hay, William W., Jr
• Format: Journal Article
• Language: English
• Published: United States 01.04.2002
• Subjects: Age Factors; Animal Nutritional Physiological Phenomena; Animals; Blood Glucose - metabolism; Body Weight; Female; Fetal Growth Retardation - physiopathology; Oxygen Consumption - physiology; Placenta - blood supply; Pregnancy; Pregnancy Outcome; Regional Blood Flow - physiology; Umbilical Veins - physiology; Uterus - blood supply
• ISSN: 0363-6119; 1522-1490
• DOI: 10.1152/ajpregu.00465.2001

1  The Rowett Research Institute, Bucksburn, Aberdeen AB21 9SB, United Kingdom; and 2  Division of Perinatal Medicine, University of Colorado School of Medicine, Denver, Colorado 80262 To establish physiological mechanisms for fetal growth restriction in pregnant adolescent ewes we studied uterine, fetal, and uteroplacental metabolism in ewes offered a high ( n  = 12) or moderate ( n  = 10) dietary intake. High intakes decreased placental (226 vs. 414 g, P  < 0.001) and fetal weight (3,323 vs. 4,626 g, P  < 0.01). Uterine blood flow was reduced absolutely ( 36%) but proportional to conceptus weight; umbilical blood flow was reduced absolutely ( 37%) and per fetal weight ( 15%). Uterine oxygen uptake was decreased per conceptus weight ( 14%); there was no change in fetal weight oxygen consumption. Uteroplacental oxygen consumption and clearance were reduced proportional to weight. Similar changes were measured for glucose fluxes and fetal glucose concentration; fetal insulin concentration was reduced. In this model of fetal growth restriction, therefore, maintenance of fetal weight-specific glucose and oxygen consumption rates are producing relative hypoglycemia and hypoxemia. This indicates that increased fetal glucose clearance and/or insulin sensitivity may be operating as compensatory mechanisms to preserve normal fetal metabolism while fetal growth is sacrificed. uterine blood flow; umbilical blood flow; placenta; fetus; intrauterine growth restriction