[The situation of pathological anatomy in France].
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Biomedical subjects
Publications and source records attributed to L Orcel.
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On the basis of a histological study of vascular lesions of the endometrium following 108 cases of spontaneous abortion, the authors propose the following conclusions: 1) In the first six weeks of pregnancy, early abortion results more often from a primary ovular defect than from any abnormality in the maternal environment, of endogenous or exogenous origin and capable of resulting in a lesion of the endometrium or its vascularisation. The structure of the walls of the spiral arteries of pregnancy is almost invariably normal. 2) By contrast, in late abortions, arterial lesions--and in particular fibrosis--may play a role. This occurs however when the basal arteries with a well-differentiated elastic structure are involved. The spiral arteries of pregnancy and the utero-placentar arteries are involved only by lesions of vasculitis secondary to inflammatory phenomena as a result of retention of the products of conception or by pseudo-atheromatous lesions resulting from the deposition of degenerated cyto-trophoblastic elements, but never from true arteriosclerotic lesions.
It appears that the classical concept of atherosclerosis cannot be applied indiscriminately to all cases and that it is essentially valid for the aorta and its large branches of predominantly elastic structure. When more peripheral arterial trunks are considered, those of muscular type, the lesions are in great part characterized by a dystrophic fibrosis of the media, associated with a diffuse intimal thickening and with stratified fibro-hyaline plaques narrowing the lumen; the latter are responsible for the circulatory insufficiency and gangrene. Comparative analysis of 50 surgical specimens allow us to conclude that those fibro-hyaline plaques represent progressively stratified parietal thrombi that are populated by myocytes, at the contact of which ultrastructural investigation reveals important phenomena of elastogenesis and elastolysis. Most probably, the myocytes originate from the media, through fenestration within the inner elastic membrane. These facts have more than just a purely speculative interest: they express the great plasticity of the arterial walls and their capacity of adaptation to new hemodynamic and biologic conditions. It is interesting to note that this lesion constantly presents signs of metabolic activity and structural remodeling despite its long standing caracter.
The authors report their preliminary results of a study of the possible therapeutic activity of a titrated extract of Centella asiatica in chronic hepatic disorders. Early results are encouraging, especially from a histological point of view, where improvement in the criteria evaluated was noted in 5 of the 12 patients treated for the longest time. These results have to be assessed in a critical manner until confirmation is obtained by complementary studies.
The work of Small and al. concerning the physical state of lipids accumulated in atherosclerotic plaques, is analysed. This team of biophysicists studies the composition in cholesterol, cholesterol esters and phospholipids, of each type of lesion and reports it on a phase diagram, while identifying the physical state of these lipids by polarizing microscope and by X-ray diffraction. In such a way, they show that the ordinary fatty streak has a composition which situates it in the 2 phases-zone, and actually demonstrate liquid crystals of phospholipids (+ cholesterol + cholesterol esters) and oily droplets of cholesterol esters, but never cholesterol crystals. In the other types of lesions (intermediary lesions, fibrous plaques and atheromatous plaques) they find, in addition to liquid crystals and oily droplets previously mentioned, crystals of cholesterol monohydrate, which leads to 3 phases. These findings are in accord with experimental models studied by the authors, for whom the physical state of lipids plays a very important role in the formation as well as the regression of atherosclerotic plaques.
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Retro-placental haemorrhage comes from rupture of patent utero-placental arteries which are neither sclerosed nor thrombosed. This applies whether the form of haemorrhage is minor (simple depression found when the placenta is examined) or grave with utero-placental apoplexy (with complete detachment of the placenta and syndrome of shock). The method by which the arteries rupture depend on the intensity and excessive duration of uterine contractions: --moderate; normal uterine contractions give rise to a prolonged blockage of the return circulation, whereas the arterial flow has not stopped. Rupture occurs because the distended utero-placental arterial wall bursts under the insult of raised pressure during the uterine contraction; --intense; these anomalies come from total blockage, both veinous and arterial, and the arterial rupture is due to anoxaemic necrosis of the utero-placental arterial wall. The rupture of the utero-placental arterial wall, which is normally very fragile because it has no elasticity in its musculature, gives the explanation for the histogenesis of retro-placental haemorrhages.