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Biomedical subjects

G Dixon

Publications and source records attributed to G Dixon.

68 records · Page 4Linked to original sources
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↗
PubMedDate not supplied

Trophoblastic invasion of human decidua from 8 to 18 weeks of pregnancy.

Trophoblastic invasion of the human decidua has been studied in 48 intact uteri with pregnancies ranging from 8 to 18 weeks after the last menstrual period. Some cytotrophoblast invades the distal segments of the spiral arteries to become endovascular while the rest diffusely infiltrates the decidua as an interstitial invader. The interstitial cytotrophoblast reaches the myometrium and gives rise to the characteristic placental bed giant cells. As the placental site enlarges the lateral spiral arteries come to lie obliquely; new openings into the intervillous space are created but this readjustment of the placental blood supply may cause focal superficial decidual necrosis. The physiological changes converting the spiral to the uteroplacental arteries are effected in the upper decidua by the action of endovascular and perivascular cytotrophoblast, whereas in the deeper decidua endovascular trophoblast is principally involved. Endometrial granulocytes aggregate in the region of maternal tissue degeneration with the heaviest trophoblast invasion but the role played by these cells in placentation is unknown.

Arteries↗
PubMedDate not supplied

The pattern of interstitial trophoblastic invasion of the myometrium in early human pregnancy.

The human placental bed myometrium, studied in 42 intact hysterectomy specimens ranging from 8 to 18 weeks' gestation, is characterized by the presence of large numbers of non-villous invasive cytotrophoblastic cells. Quantitative morphometric analysis reveals a tendency for maximal invasive activity to occur at the centre and, subsequently, to extend centrifugally to produce an annular pattern. Morphological observations suggest that the intimate mixture of cytotrophoblast with myometrial tissue must affect the mechanical properties of the myometrium. Local hormone production by trophoblast may induce or enhance these and other changes in uterine tissues that are essential for the establishment of human placentation. Cytotrophoblastic invasion into the myometrium appears to be restricted to the earlier stages of gestation and morphological evidence indicates that, subsequently, clumps of cytotrophoblast fuse to form multinuclear syncytiotrophoblast, the characteristic placental bed giant cells.

Female↗
PubMedDate not supplied

Review article: trophoblast invasion and the establishment of haemochorial placentation in man and laboratory animals.

Trophoblast invasion is an essential component of haemochorial placentation and has to be considered to relation to reactive changes in the maternal uterine tissues. Some comparative aspects of human and laboratory rodents are discussed and, although there is an obvious phylogenetic gap between the two, many characteristics of placental development are found to be analogous. Trophoblast growth into the uterus is different in different species: localized trophoblast growth forming a bulky tissue (mouse, rat, hamster) contrast with a dispersion of independent trophoblastic elements, forming an interstitial invasion (guinea pig, man). In the rat, mouse, hamster and man retrograde intra-arterial trophoblast migration occurs in maternal vessels supplying blood to the developing placenta. Early changes in maternal tissue might influence trophoblast behaviour. Decidualization probably is a key phenomenon, and the relation of decidual necrosis to trophoblast invasion is considered. Some kind of controlled immune response by the mother also may be involved. These considerations apply to stromal or interstitial invasion as well as to intravascular trophoblast migration but, for the latter, haemodynamic factors probably influence tissue reactions.

Adaptation, Physiological↗