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Biomedical subjects

W B Robertson

Publications and source records attributed to W B Robertson.

At least 37 records · Page 2Linked to original sources
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

Pathology of acute myocardial infarction with particular reference to occlusive coronary thrombi.

Analysis of the pathological findings in 500 cases of fatal acute myocardial infarction showed that in 469 this was localized to one transmural area of the left ventricle; in 31 there was diffuse subendocardial necrosis. In the former occlusive coronary thrombus was found in the related artery in 95 per cent of cases. Variation in the percentage of occlusions found was noted between different prosectors and when coronary artery calcification was present. Only 4 of the 31 patients with subendocardial necrosis had recent occlusion; triple vessel disease was common in this group suggesting general failure of coronary perfusion. It is essential in necropsy studies of the relation of coronary thrombosis to myocardial infarction to be sure that muscle necrosis is present, to distinguish the two forms of myocardial necrosis, and to employ a meticulous dissection technique with decalcification of the arteries when necessary.

Acute Disease↗
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 ultrastructure of organising experimental mural thrombi in the pig aorta.

This ultrastructural study of experimentally produced mural thrombi in the pig aorta has shown that at 3 days there are, amongst the other constituents, two distinct cell populations, macrophages and undifferentiated mesenchymal cells. Over the subsequent 2 wk the mesenchymal cells, which appear to be homogeneous initially throughout the thrombus, gradually differentiate on the surface to form an endothelial lining, in the superficial layers to form myointimal cells and ultimately smooth muscle and, in the deeper layers, to form new capillaries which join with endothelial lined clefts from the surface. The morphological evidence supports the postulate that the early stage of organisation of a mural thrombus in effected by pluripotent precursor cells from the circulating blood. The new endothelium, myointimal cells, capillaries, intimal smooth muscle and the extracellular tissues characteristic of an organising thrombus all appear to derive from this common source. In this study we saw no evidence to suggest that, at this stage, there was a contribution from the cells native to the vessel wall which, however, may be involved in the later stages of organisation.

Animals↗
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↗
PubMed1974

Assessment of incremental dosage regimen of combined oestrogen-progestogen oral contraceptive.

Eighty-six women of proved fertility used an incremental dosage regimen of a combined oral contraceptive for a total of 570 cycles over one year. A daily tablet containing 50 mug of ethinyloestradiol and 50 mug D-norgestrel was taken for 11 days and a daily tablet containing 50 mug ethinyloestradiol and 125 mug D-norgestrel for the next 10 days. Withdrawal bleeding occurred during the tabletfree interval of seven days. The new preparation proved to be an efficient contraceptive, well tolerated, and with few side effects. Women who had gained weight while taking other oral contraceptives lost weight when they changed to the new preparation. The regimen allowed a significant reduction in the cycle dose of progestogen, and these results suggest that a further reduction in the cycle dose of both oestrogen and progestogen may be possible without losing contraceptive efficiency.

Biopsy↗