Using kidneys from diabetic patients, the morphogenesis of elastic hyperplasia (“laminated elastosis”) in the intrarenal arteries was studied by electron microscopy. In the thickened intima, myointimal cells produced ground substance, collagen fibers and elastic tissue. The elastic tissue was stained black electron microscopically with orcein. Newly‐formed elastic tissue in the intima was first found on either the basement membrane or basement membrane‐like materials around the myointimal cells and endothelial cells. Subsequently, small areas of elastic tissue aggregated and fused to form larger areas of elastic tissue or concentric thick elastic laminae, the latter containing a large number of collagen fibrils. Upon treatment with elastase, newly‐formed elastic tissue was digested, but the microfibrillar component remained unstained.
The bifurcation pads ("valve-like projections") in the anterior cerebral arteries of rats with long-term hypertension were studied electron microscopically. The rats ranging in age from 2 to 10 months were sacrificed after bilateral renal artery constriction at 5-week-old. In the bifurcation pads (intimal pads) of hypertensive rats, smooth muscle cell damage first appeared in the roots of the pads as well as underlying media in the form of granular, vesicular, and somewhat tubular structures (200-1500 A in diameter).Thereafter, with a lapse in time after the operation, these abnormal substances increased around the smooth muscle cells which were arranged in the marginal zones of the pads. Deeply arranged intimal smooth muscle cells which were embedded in an abundance of ground substances were only damaged in rats with very long-term hypertension. The medial smooth muscle cells beneath the pads manifested lesions which were more marked and diffuse than in the intima. These smooth muscle cells were bizarrely atrophied and abnormal substances which might be derived from necrotic smooth muscle cells were found around them. Basement membrane-like substances, either thick or multilaminated, were also present around them. ACTA PATHOL. JPN. 32: 31-39, 1982.
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RIFURCATIONS I N HYPERTENSIVE RAT ARTERIESAcfa Pathol. Jpn.
Changes in the middle cerebral arteries, especially in the media, of rats with experimental hypertension were electron microscopically studied. The animals whose brains showed gross hemorrhage or softening were excluded.Medial smooth muscle cells exhibited focal cytoplasmic degradation, and most of the necrotic parts were found in autophagic vacuoles. vacuoles which resulted from disposal of the degraded cytoplasm in the autophagic vacuoles. The disposed necrotic parts, discharged out of the cells were seen as vesicles varying in size around the smooth muscle cells. The medial smooth muscle cells became smaller as if torn off, and finally disappeared. ACTA PATH. JAP. 20: 399-408, 1970.Medial lesions were severer than intimal ones.There were also
The fine structure of capillary hemangiomas from the skin of six young adults was investigated. All the vessels had non‐fenestrated endothelial cells. Their intercellular junctions had tight junctions, but desmosome‐We structures were also present. Cytoplasmic filaments (50–100Å in width) as well as microtubular bodies were present in some of the endothelial cells. The bodies were approximately 0.1 μm in diameter and up to 0.5 μm in length. Sub‐endothelial basement membrane was present and sometimes multilaminated. Pericytes had a feature of endothelial cells, fibroblasts, or smooth muscle cells. “Fibrous long‐spacing collagen fibrils” (periodicity: 700–1500Å) were seen in the vicinity of pericyte basement membranes or in the intervascular spaces.
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