Premium
Chronic Hypoxia Elevates Fetoplacental Vascular Resistance
Author(s) -
Jakoubek Vit,
Bibova Jana,
Venclikova Kvetoslava,
Hampl Vaclav
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1217-c
Subject(s) - hypoxia (environmental) , vascular resistance , cardiology , medicine , biology , chemistry , oxygen , hemodynamics , organic chemistry
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.