title: Chronic hypoxia increases fetoplacental vascular resistance and vasoconstrictor reactivity in the rat.
abstract: An increase in fetoplacental vascular resistance caused by hypoxia is considered one of the key factors of placental hypoperfusion and fetal undernutrition leading to intrauterine growth restriction (IUGR), one of the serious problems in current neonatology. However, although acute hypoxia has been shown to cause fetoplacental vasoconstriction, the effects of more sustained hypoxic exposure are unknown. This study was designed to test the hypothesis that chronic hypoxia elicits elevations in fetoplacental resistance, that this effect is not completely reversible by acute reoxygenation, and that it is accompanied by increased acute vasoconstrictor reactivity of the fetoplacental vasculature. We measured fetoplacental vascular resistance as well as acute vasoconstrictor reactivity in isolated perfused placentae from rats exposed to hypoxia (10% O(2)) during the last week of a 3-wk pregnancy. We found that chronic hypoxia shifted the relationship between perfusion pressure and flow rate toward higher pressure values (by approximately 20%). This increased vascular resistance was refractory to a high dose of sodium nitroprusside, implying the involvement of other factors than increased vascular tone. Chronic hypoxia also increased vasoconstrictor responses to angiotensin II (by approximately 75%) and to acute hypoxic challenges (by >150%). We conclude that chronic prenatal hypoxia causes a sustained elevation of fetoplacental vascular resistance and vasoconstrictor reactivity that are likely to produce placental hypoperfusion and fetal undernutrition in vivo.
authors.affiliation: Dept. of Physiology, Charles University, Plzenská 130/221, 15000 Prague 5-Motol, Czech Republic.
authors.forename: Vít
authors.initials: V
authors.lastname: Jakoubek
authors.forename: Jana
authors.initials: J
authors.lastname: Bíbová
authors.forename: Jan
authors.initials: J
authors.lastname: Herget
authors.forename: Václav
authors.initials: V
authors.lastname: Hampl
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001783:Blood Flow Velocity; D001794:Blood Pressure; D002908:Chronic Disease; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005260:Female; D005317:Fetal Growth Retardation / Q000209:etiology* / Q000503:physiopathology; D005865:Gestational Age; D000860:Hypoxia / Q000150:complications / Q000503:physiopathology*; D009599:Nitroprusside / Q000494:pharmacology; D021041:Placental Circulation / Q000187:drug effects; D011247:Pregnancy; D051381:Rats; D017208:Rats, Wistar; D012039:Regional Blood Flow; D014655:Vascular Resistance / Q000187:drug effects; D014661:Vasoconstriction / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D000804:Angiotensin II; D009599:Nitroprusside