Fetoplacental Vascular Resistance is Elevated by Experimental Diabetes and Hypoxia

Abstract

Acute and chronic hypoxia during the last part of pregnancy increases fetoplacental vascular resistance (Hampl & Jakoubek, Physiol Res 58: S87, 2009). Hypoxic hypoperfusion of the fetal side of the placenta is commonly considered causative in the syndrome of impaired fetal growth. Since maternal diabetes is a well‐known factor affecting fetal growth, we tested the hypothesis that maternal diabetes affects fetoplacental vascular resistance. Diabetes was induced in rats by a single injection of streptozotocin (50 mg/kg i.p.) on day 14 of pregnancy (term = 21 days). One of the placentae from each dam was prepared on day 20 and both its maternal and fetal side was perfused ex vivo with Krebs solution while fetoplacental perfusion pressure (FPPP) was measured. At constant flow rate (1 ml/min), FPPP was higher by 14% in the diabetic (D) than in the control (C) placentae (26 vs. 22 mmHg, P>0.05). Acute hypoxia increased FPPP in C (by 22%, P>0.001) and significantly less so in D (by 8%, P>0.05). During acute hypoxia FPPP did not differ between C and D. The results were similar in a different model of diabetes (100 mg/kg streptozotocin given on second postantal day to future mothers). Using this model, we also found that diabetes markedly potentiated the rise in fetoplacental vascular resistance caused by chronic hypoxia (10% O2 for the last week of pregnancy). These data indicate that experimental diabetes increases fetoplacental vascular resistance to a similar extent as acute hypoxia and potentiates the effect of chronic hypoxia.Supported by Grant Agency of the Czech Republic grant # 13‐01710S.