AB: Placental bed biopsies taken during caesarean section from 10 patients with pre-eclampsia and six healthy pregnancies were studied. We applied antibodies against cytokeratin and different macrophage markers to analyse the distribution of invasive extravillous trophoblast cells as compared to that of macrophages in myometrial segments of uteroplacental arteries. The data were evaluated quantitatively. We found a clear inverse relationship between local infiltration with macrophages and trophoblast invasion. In pre-eclampsia, vessel cross-sections prevailed which were characterized by large numbers of macrophages but a low degree of trophoblast invasion. In contrast, in normal third trimester pregnancies the respective arterial segments had a high degree of trophoblast invasion but were largely void of macrophages. These data suggest causal links between macrophages and inhibition of intra-arterial trophoblast invasion in pre-eclampsia.
: Плацентарные биопсии кровати, принятые в течение секции монархиста от 10 пациентов с преэклампсией и шестью здоровыми беременностями были изучены. Мы применили антитела против cytokeratin и различных макрофагальных маркеров, чтобы анализировать распределение инвазивного extravillous trophoblast ячейки по сравнению с таковым макрофагов в сегментах myometrial uteroplacental артерий. Данные были оценены quantitatively. Мы нашли ясные обратные отношения между местной инфильтрацией с макрофагами и trophoblast вторжением. В преэклампсии, взаимные секции сосуда преобладали, которые были характеризованы большими количествами(номерами) макрофагов, но низкой степени(градуса) trophoblast вторжения. Напротив, в нормальных третьих беременностях триместра соответствующие артериальные сегменты имели высокую степень(градус) trophoblast вторжения, но были в значительной степени лишены из макрофагов. Эти данные предлагают причинные связи между макрофагами и запрещением внутриартериального trophoblast вторжения в преэклампсии.
TI: U46619-mediated vasoconstriction of the fetal placental vasculature in vitro in normal and hypertensive pregnancies.
: U46619 - Опосредованная вазоконстрикция эмбриональной плацентарной сосудистой сети in itro в нормальных и гипертензивных беременностях.
AU: Read-MA; Leitch-IM; Giles-WB; Bisits-AM; Boura-AL; Walters-WA
AD: Division of Obstetrics and Gynaecology, John Hunter Hospital, Newcastle, New South Wales, Australia. mdmar@mail.newcastle.edu.au
SO: J-Hypertens. 1999 Mar; 17(3): 389-96
CP: ENGLAND
AB: OBJECTIVES: To measure in-vitro responses to the thromboxane A2 (TxA2) mimetic U46619 in the fetal placental vasculature of human placentae from normotensive women and those with pre-eclampsia. Furthermore, to compare fetal vascular responses to endothelin-1,5-hydroxytryptamine, potassium chloride (KCl) and prostacyclin (PGI2) in placentae from normal or pre-eclamptic pregnancies. METHODS: Single placental lobules of intact placentae were bilaterally perfused in situ (fetal and maternal) with constant flows of Krebs' solution. Changes in fetal arterial perfusion pressure during intra-arterial infusion of vasoactive agents were recorded. Fetal placental vasoconstrictor concentration response curves were obtained to U46619 (0.01-300 nmol/l), endothelin-1 (0.4-160 nmol/l), KCl (3-300 mmol/l) and 5-hydroxytryptamine (0.03-30 mumol/l). In addition, vasodilator concentration response curves were obtained for PGI2 (1.2-350 nmol/l) in the fetal placental circulation during submaximal increases in perfusion pressure with prostaglandin F2 alpha (PGF2 alpha; 0.7-2.0 mumol/l). RESULTS: The maximum increase in perfusion pressure caused by U46619 in placentae from normotensive women was 194 +/- 25 mmHg. The maximum response to U46619 was significantly reduced in the placentae from women with pre-eclampsia (104 +/- 21 mmHg). In contrast, there were no differences in constrictor responses to endothelin-1,5-hydroxytryptamine and KCl, or in dilator responses to PGI2 in placentae obtained from either normotensive women or those with pre-eclampsia. CONCLUSION: TxA2 receptor-mediated vasoconstriction is reduced in the fetal vasculature of placentae from women with pre-eclampsia, possibly to compensate for the increased levels of TxA2 seen in these conditions.
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