Chronic Hypoxia Elevates Fetoplacental Vascular Resistance

Hypoxia of the placenta (e.g. in preeclampsia) is commonly considered a key pathogenetic factor in the development of intrauterine growth restriction, a serious problem in neonatology. While acute hypoxia has been shown to induce vasoconstriction in the fetal side of the placenta ( 1 ), the effect of chronic hypoxia – most relevant clinically – has never been systematically studied. We exposed rats to normobaric hypoxia (10% O2) during the last week of the 3‐week pregnancy. One day before the expected date of delivery, they were anesthetized with Thiopental,50mg/kg IP. One placenta was dually perfused (from both the maternal and fetal side) ( 2 ) with Krebs saline gased with 21%O2+5%CO2+74%N2. To characterize fetoplacental resistive properties, the pressure‐flow relationship (P/Q) was evaluated by measuring perfusion pressure while increasing flow rate in 0.2 ml/min steps. The pressure axis intercept of the P/Q linear regression was higher in the hypoxic (7.8±1.3 mmHg) than the normoxic rats (3.6±1.0 mmHg, P<0.02). The slopes did not differ. The P/Q lines were unaltered by high dose of sodium nitroprusside in either group. We conclude that chronic hypoxia causes elevation of fetoplacental vascular resistence resistant to vasodilators. Supported by GACR 305/04/1327 and GAUK 82/2004/C.