Cerebral oxidative metabolism during intrauterine growth retardation

Biology of the Neonate
J D Brown, R C Vannucci

Abstract

Cerebral oxidative metabolism during intrauterine growth retardation was investigated utilizing a pregnant-rat model. Dams were subjected to unilateral uterine artery ligation on the 17th day of gestation. At term, they were sacrificed by decapitation and the fetuses delivered by cesarean section. Body and brain weights of fetuses from ligated uterine segments were smaller than those of offspring from nonligated horns of the experimental rats or those from sham-operated dams. Blood glucose at birth was reduced by 25% in growth-retarded fetuses. Cerebral oxidative metabolites, including glycogen, glucose, lactate, ATP, and phosphocreatine, were not different from control levels. These findings suggest that neither tissue hypoxia nor deficient glucose delivery to brain can account for the stunted cerebral growth observed in fetuses following uterine artery ligation.

Citations

Jan 1, 1988·International Journal of Developmental Neuroscience : the Official Journal of the International Society for Developmental Neuroscience·M Bisignano, S Rees
Jan 1, 1992·Journal of Perinatal Medicine·M Thordstein, U A Nilsson
Nov 27, 2015·The Journal of Physiology·Suzanne L MillerCarina Mallard
Oct 23, 1998·Experimental and Toxicologic Pathology : Official Journal of the Gesellschaft Für Toxikologische Pathologie·R BauerU Zwiener
Mar 1, 1990·Early Human Development·W H TrescherR C Vannucci
May 1, 1986·Journal of Neurochemistry·A FuglsangA Gjedde

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