Obstetrics and gynecology · 1993
Fetal endothelin levels and placental vascular endothelin receptors in intrauterine growth retardation.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
McQeen J, Kingdom J C, Connell J M, Whittle M J
Аннотация
OBJECTIVE: To examine endothelin 1 (ET-1) in normal pregnancies and those complicated by severe intrauterine growth retardation (IUGR) with normal or increased fetoplacental vascular resistance as assessed by umbilical artery Doppler flow velocimetry.
METHODS: Endothelin 1 concentrations were measured by radioimmunoassay in fetal umbilical arterial and venous and maternal venous plasma, and vascular ET-1 receptors were quantified by radioligand binding methods in placental primary and secondary stem villous vessels.
RESULTS: Fetal and maternal ET-1 concentrations were similar in normal pregnancy (10-15 pmol/L) and were not influenced by mode of delivery (vaginal versus cesarean). Fetal levels were identical to control values in the growth-retarded fetuses with normal umbilical artery flow, but were markedly elevated (above 50 pmol/L) in two cases with increased fetoplacental vascular resistance. The corresponding maternal levels also appeared elevated, but to a lesser extent. Endothelin receptors were identified in placental vascular tissue. No differences in receptor-binding characteristics were observed between the groups.
CONCLUSION: The increased fetoplacental vascular resistance present in a proportion of pregnancies complicated by severe IUGR may be associated with elevated fetal plasma ET-1 concentrations, but with no apparent change in vascular sensitivity to the peptide.
METHODS: Endothelin 1 concentrations were measured by radioimmunoassay in fetal umbilical arterial and venous and maternal venous plasma, and vascular ET-1 receptors were quantified by radioligand binding methods in placental primary and secondary stem villous vessels.
RESULTS: Fetal and maternal ET-1 concentrations were similar in normal pregnancy (10-15 pmol/L) and were not influenced by mode of delivery (vaginal versus cesarean). Fetal levels were identical to control values in the growth-retarded fetuses with normal umbilical artery flow, but were markedly elevated (above 50 pmol/L) in two cases with increased fetoplacental vascular resistance. The corresponding maternal levels also appeared elevated, but to a lesser extent. Endothelin receptors were identified in placental vascular tissue. No differences in receptor-binding characteristics were observed between the groups.
CONCLUSION: The increased fetoplacental vascular resistance present in a proportion of pregnancies complicated by severe IUGR may be associated with elevated fetal plasma ET-1 concentrations, but with no apparent change in vascular sensitivity to the peptide.