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Biomedical subjects

P Fabbrini

Publications and source records attributed to P Fabbrini.

At least 19 recordsLinked to original sources

Ultrastructural aspects of cynomolgus atherosclerotic carotid artery lesions on cholestyramine 'regression' treatment.

The carotid artery lesions of atherosclerotic cynomolgus monkeys treated with cholestyramine and studied with scanning electron microscopy appeared to be less bulging and largely covered by endothelial cells. With transmission electron microscopy these lesions showed an evident disappearance of cells and of extra- and intracellular lipid; a marked relative increase of fibrous material in the intercellular matrix, chiefly collagen and elastin fibers, was noted.

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[Preliminary observations, at the ultrastructural level, on the reactivity of cerebral arteries from New Zealand rabbits to combined atherogenic stimuli (hypercholesterol diet and hypertension)].

Both in monkeys (Rhesus and Cynomolgus) and in New Zealand rabbits fed an atherogenic diet, a marked delay in the appearance of atherosclerotic lesions of the cerebral arteries in comparison with other arterial districts has been observed. This appearance has been described in monkeys as relatively earlier if hypertension is added to the atherogenic diet. Preliminary observations on a little group of rabbits on a 3 months hypercholesterolic diet, subjected to Goldblatt aortic coarctation, have shown an increase of blood pressure and a severe gross atherosclerotic involvement of aorta, resembling the one obtainable after 6 months of atherogenic diet. Histologically, the aorta predominantly shows lesions of the fatty streaks type with necrotic areas in the deep; the carotid lesions show some lipid in smooth muscle cells disseminated in a sub-endothelial "edematous" space (rich in protein). The cerebral arteries do not show any lesion. At TEM, the aortic lesions look sometimes as advanced plaques with an initial fibrosis at the surface; the carotid lesions are characterized by a granular deposit in the sub-endothelial space in which some smooth muscle cells (with lipid in the cytoplasm) are present; in the cerebral arteries only the presence of collagen fibers among the smooth muscle cells of the media, never observed in the animals fed the atherogenic diet alone, has sometimes been noted.

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An ultrastructural comparison of diet-induced atherosclerosis of arteries supplying the central nervous system in cynomolgus and rhesus monkeys.

The carotid lesions of cynomolgus and rhesus monkeys fed an 8- to 12-months atherogenic diet are very severe. However, the basilar, vertebral and middle cerebral arteries of the same atherosclerotic monkeys look instead, at SEM examination, similar to the control ones. At TEM examination, these arteries of the atherosclerotic monkeys show only minimal lesions in the subendothelial space ('edema' and presence of fragments of basilar membrane) and sometimes necrobiosis of endothelial cells. The smooth muscle cells, which are also present in the controls in these arteries in the subendothelial space, are sometimes surrounded by a nest of basement membrane beads and do not contain lipid droplets.

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[Preliminary data on the different endothelial reaction to Con A at different levels of the arterial tree in rabbits and in Cynomolgus monkeys].

Delayed appearance of atherosclerotic lesions in cerebral arteries has been observed not only in man but also in monkeys and rabbits submitted to atherogenic diets. Previous observations of ours had shown a Con A positive reaction ("glycocalyx" or "surface coat") at the luminal surface and in the plasmalemmal vesicles of aortic endothelial cells of rabbits an other laboratory animals. The "surface coat" is now reputed the site of lipoproteinlipase activity whose importance in atherogenesis has recently been stressed. In our present observations, the endothelial cells Con A reactivity after Bernhard and Avrameas which was not previously studied in the cerebral arteries of rabbits and monkeys has resulted always lacking in this arterial district. Those observations may help explaining delayed appearance of atherosclerotic lesions in cerebral arteries.

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Aortic surface coat scanning electron-microscopic modifications after short-term hypercholesterolic diet, visualized in rabbits by con A-haemocyanin reaction.

Modifications of the aortic endothelial surface coat have been visualized at SEM with the use of the Con A-haemocyanin method. After fifteen days of an atherogenic diet, a strong increase of the reactive coat was evident in areas near the orifice of the collateral branches. In other areas, the reaction appeared to be intensely diminished.

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Regression of arteriosclerotic lesions in rhesus monkey aortas after regression diet. Scanning and transmission electron microscope observations of the endothelium.

Scanning and transmission microscopy were used to study aortic intima atherosclerotic lesions in Rhesus monkeys during both progression and regression phases. Scanning micrographs of severely atherosclerotic lesions showed areas of disjunctive endothelium and discontinuous basement membranes, frequently accompanied by red blood cells and other circulating elements adhering to the surface. Transmission micrographs also showed occasional areas of endothelial cell damage and loss with lipid-laden smooth muscle cells and foam cells beneath. Regressed lesions (affected by low-fat, low-cholesterol diet with or without cholestyramine) showed endothelial changes suggestive of reparative processes. Scanning micrographs showed flattened residual lesions with continous endothelial lining, while transmission microscopy disclosed interdigitated intercellular tight junctions and frequently reduplicated basement membranes.

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Aortic endothelial and sub-endothelial lesions in early stages of experimental atherogenesis and in scurvy.

The endothelial and sub-endothelial lesions during early stages of experimental atherogenesis and scurvy have been studied by means of scanning EM and transmission EM, making use also of the Con-A reaction. The surface coat modifications were accompanied by formation of vacuoles in the endothelial cells and by sub-endothelial 'oedema', not only in rabbits fed a hypercholesterolic diet but also in scorbutic guinea pigs. The endothelial lesions were sometimes found even before clear modifications of the Con-A surface reactive layer were apparent.

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