The Modulation of Glucose Transfer Across the Human Placenta by Intervillous Flow Rates: An In Vitro Perfusion Study
There is substantial evidence that a high proportion of fetal growth retardation in man is the result of uteroplacental vascular insufficiency. The association of growth retardation with maternal hypertensive disease, cyanotic heart disease and the relationship between growth retardation and low prepregnancy blood volume support the suggestion that chronic flow restriction may result in intrauterine growth retardation (Seeds, 1984). At the same time, in cases of essential hypertension and pre-eclampsia, a reduction in uteroplacental blood flow of 50–60% has been demonstrated (Brown and Veall, 1953; Lunell et al., 1979). Blood flow in growth retarded pregnancies can be reduced by over 50%, even in those women who do not display signs of hypertensive disorders or fetal malformations (Nylund et al., 1983).
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