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Biomedical subjects

I Brosens

Publications and source records attributed to I Brosens.

At least 91 records · Page 5Linked to original sources
PubMed1980

Fetal growth retardation and the maternal arterial supply of the human placenta in the absence of sustained hypertension.

In five patients with fetal growth retardation in pregnancies with no or only a moderate and transient rise in blood pressure, vascular lesions in the placental bed spiral arteries were found. These lesions are characterized by less well developed physiological morphological changes, by extensive intimal thickening, by fibrinoid degeneration of the media and by acute atherosis. the recurrent fetal growth retardation in these pregnancies may be the first clinical manifestation of underlying reno-vascular disease.

Adult↗
PubMed1978

Microanatomy of the human amniotic membranes. A light microscopic, transmission, and scanning electron microscopic study.

The human amnion was examined by means of light microscopy and scanning and transmission electron microscopy. The surface shows apart from microvilli a particular structure, called "blebs"; the intercellular junction is formed by desmosomes and a labyrinthine channel system, and at the base pedicels extend into the basement membrane. Cell shedding uncovers the basement membrane which seems to play a primordial role in preserving the intact amniotic cavity. These data underline the complex structure and the multiple role the amnion performs during gestation.

Amnion↗
PubMed1977

Fetal growth retardation and the arteries of the placental bed.

The morphology of the placental bed spiral arteries was studied in 68 pregnancies complicated by fetal growth retardation and in 40 pregnancies with a normally grown fetus. When the birth weight was normal the extent and depth of physiological vascular changes were normal except in those pregnancies complicated by pre-eclampsia. When the birth weight was low and the mothers were normotensive the extent and depth of physiological vascular changes were either normal or restricted, and in all patients with hypertension and a baby with low birth weight the physiological changes were restricted to the decidual segments of the spiral (uteroplacental) arteries. Acute atherosis was only found in pregnancies complicated by hypertension, particularly if there was proteinuria. We do not believe that there exists an arteriopathy which is common to hypertensive and normotensive pregnancies complicated by fetal growth retardation.

Arteries↗
PubMed1976

Secretion rates of LH and FSH during infusion of LH-FSH/RH in normal women and in patients with secondary amenorrhea: suggestive evidence for two pools of LH and FSH.

Normal women in the early follicular phase and in the luteal phase of the cycle, and patients with secondary amenorrhea received on consecutive days a rapid intravenous injection (50 mug) and a two or four-hour infusion (25 mug/h) of synthetic LH-FSH/RH. The responses of LH and FSH were evaluated by the measured plasma concentrations, as well as by the calculated pituitary secretion rates and by the amounts of hormone released. To estimate these pituitary secretion rates of LH and FSH, a simplified mathematical model is proposed. During an infusion of LH-FSH/RH the secretion rates of both LH and FSH increased in the three groups of women in a biphasic way with a dip after 1 to 2h of infusion, suggesting that besides the pool mobilized by a rapid intravenous injection of LH-FSH/RH there is a second pool of (stored) gonadotropins. For LH the increase above baseline concentrations was higher in group II (luteal phase) than in group I (follicular phase) or in group III (amenorrhea) and this both after a bolus injection and during infusion of LH-FSH/RH. For FSH a similar pattern of response prevailed during an infusion of LH-FSH/RH. After a bolus administration, however, the FSH release was relatively higher in group III (amenorrhea) than in both groups of normal women in which the increases were about the same. The latter finding suggests that the first pool of FSH is released by a different mechanism than the second pool.

Adult↗
PubMed1976

Maternal uterine vascular lesions in the hypertensive complications of pregnancy.

To establich hemochorial placentation, the nonvillous trophoblast breaches the spiral arteries in the basal decidua and later migrates down the arteries as far as the parent radial arteries in the myometrium. Interactions between the endovascular trophoblast and the tissues of the maternal vessel wall (physiological changes) adapt these arteries to the uteroplacental arteries, and these large caliber vessels empty into the intervillous space. Loss of reactive musculoelastic vascular tissue results in a lowering of peripheral resistance, permitting a greatly increased blood flow into the intervillous space. In preeclamptic pregnancies, there is inhibition of the secondary endovascular trophoblast migration in the second trimester, so that the myometrial segments of the uteroplacental arteries remain as responseive musculoelastic arteries. With the onset of clinical preeclampsia, acute atherosis, a necrotizing arteriopathy, affects small muscular arteries in the placental bed and arterioles in the decidua vera. When essential hypertension is complicated by preeclampsia, the placental bed arteries show a combination of hyperplastic arteriosclerosis and acute atherosis. There is evidence that the establishment of hemochorial placentation requires controlled immunological reactions between fetal and maternal tissues and that an inappropriate immune response may be involved in the pathogenesis of the arteriopathy of preeclampsia.

Arteries↗
PubMed1975

The ultrastructure of acute atherosis in hypertensive pregnancy.

Acute atherosis of the myometrial segments of the uteroplacental arteries from pre-eclamptic pregnancies was studied by electron microscopy. The lesions in their early stages are characterized by endothelial damage, insudation of plasma constituents into the vessel wall, proliferation of myointimal cells, and medial necrosis. Fat acculumation is seen first in myointimal cells and, later, macrophages engulf the lipid-rich debris released from disintegrating myogenic foam cells. Gross endothelial damage, massive intramural fibrin deposition, luminal thrombosis, and vessel rupture with hemorrhage are epiphenomena.

Arteries↗
PubMed1975

The role of ovarian steroids in placental development and endovascular trophoblast migration in the golden hamster.

Pregnant hamsters were ovariectomized on Day 7 and daily supplements of progesterone or progesterone plus oestradiol benzoate were given. Fetal development and survival was 14% and 62% respectively. Histological examination indicated that failure of labyrinthine development in the placenta resulted in failure to form an adequate number of maternal arterial spaces communicating with the base of the trophospongium to allow trophoblast migration in the related maternal spiral arteries. Progesterone was essential at all stages of gestation to sustain decidualized tissues and allow survival of a minority of fetuses. Oestradiol supplementation significantly increased fetal survival, but not to normal levels, suggesting that other oestrogens may be essential for the maintenance of normal hamster pregnancy.

Animals↗