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Am J Physiol Regul Integr Comp Physiol 263: R578-R585, 1992;
0363-6119/92 $5.00
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AJP - Regulatory, Integrative and Comparative Physiology, Vol 263, Issue 3 578-R585, Copyright © 1992 by American Physiological Society

ARTICLES

Placental glucose transport in heat-induced fetal growth retardation

P. J. Thureen, K. A. Trembler, G. Meschia, E. L. Makowski and R. B. Wilkening
Department of Pediatrics, University of Colorado School of Medicine, Denver 80262.

In six ewes heat stressed from 39 to 125 days gestation and studied in a normothermic environment at 135 days, fetal and placental masses were less than in control sheep (1,645 vs. 3,112 and 149 vs. 356 g, respectively, P less than 0.01). Umbilical glucose uptakes (Rf,UP) were measured keeping maternal arterial plasma glucose at 70 mg/dl at spontaneously occurring fetal plasma glucose values (state A) and at two additional fetal glucose levels, to determine the transplacental glucose difference (delta) vs. Rf,UP relation. At normal delta of 49.2 mg/dl, Rf,UP was less in the experimental group (3.2 vs. 5.6 mg.min-1.kg fetus-1, P less than 0.05). Differences in placental perfusion and glucose consumption could not account for this result, thus indicating a reduced placental glucose transport capacity. In state A, fetal hypoglycemia enlarged significantly (P less than 0.01) the delta to 56.7 mg/dl and increased Rf,UP approximately 50% over the Rf,UP at a normal delta. In heat-induced fetal growth retardation, fetal hypoglycemia increases the flux of maternal glucose across a placenta with reduced glucose transport capacity.


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