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Biomedical subjects

M Takatama

Publications and source records attributed to M Takatama.

24 records · Page 2Linked to original sources
PubMed1986

Role of lysosomes in coronary artery lesions of hypertensive rats.

Electron microscopically the role of acid phosphatase (acid P) positive lysosomes in the pathogenesis of intramyocardial coronary artery lesions of hypertensive rats with bilaterally constricted renal arteries was studied. At 3 postoperative weeks, acid P positive lysosomes were increased in endothelial cells of the coronary arteries, but at 5 weeks and thereafter, they were decreased in number. In the intima, intimal smooth muscle cells with acid P positive lysosomes appeared at 3 postoperative weeks, but their number remained small as late as 9 postoperative weeks. The internal elastic lamina was fragmented into amorphous masses from 3 postoperative weeks, at 5 weeks and thereafter the fragmentation and disruption became severer, and at 9 weeks the lamina disappeared because of marked disruption. At 3 postoperative weeks, acid P positive extracellular lysosomes were observed in the gaps of the fragmented internal elastic lamina. At 5 weeks and thereafter, extracellular lysosomes and attenuated processes of medial smooth muscle cells with lysosomes were seen extending through the gaps of the fragmented internal elastic lamina. Necrosis of these extending cell processes and lysosomes remaining after the necrosis were observed. The findings suggested that the fragmentation and lytic change of the internal elastic lamina observed in hypertensive rat intramyocardial coronary arteries might be induced by extracellular lysosomes discharged not only from endothelial cells and intimal smooth muscle cells but also from the extending processes of medial smooth muscle cells into the gaps of the internal elastic lamina.

Acid Phosphatase↗
PubMed1985

Light and scanning electron microscopic and immunohistochemical studies on permeability of hypertensive rat mesenteric arteries.

Experimental hypertensive rats were intravenously injected with carbon and iron as tracers, and their mesenteric arteries exhibiting hypertensive arterial lesions were observed by light and scanning electron microscopy and immunohistochemistry. Early arterial lesions showing intense medial damages, deposition of fibrinoid substance consisting of fibrin in the intima and/or media, and granulation tissue in the adventitia were characterized by marked insudation of intravenously injected tracers. Scanning electron microscopy demonstrated numerous leukocytes and platelets adhering to endothelial surface, opened endothelial cell junctions, and desquamation of these cells. Immunohistochemistry revealed laminin and low stainability of fibronectin in the subendothelium. Advanced lesions showed deposition of a large amount of fibrinoid substance and no insudation of tracers in the intima, but scanning electron microscopy manifested opening of endothelial cell junctions, desquamation of endothelial cells, and adherence of leukocytes and platelets. Immunohistochemistry revealed fibronectin in the intima and laminin just beneath the endothelium. In the healed lesions disclosing fibrocellular intimal thickening, there was no insudation of tracers. Scanning electron microscopy showed opened endothelial cell junctions, endothelial cell defects, and adherence of leukocytes and platelets. There were fibronectin in the intima and laminin beneath the endothelium. It was suggested that the opening of endothelial cells junctions and desquamation of endothelial cells would be necessary for the arterial increased permeability in hypertensive rats, and that fibrin-fibronectin complex, fibronectin-acid mucopolysaccharide complex, and basement membrane would together inhibit the increased permeability in the mesenteric arteries of hypertensive rats in spite of endothelial cell injuries and their defects.

Animals↗
PubMed1984

Endothelial changes of hypertensive rat mesenteric arteries.

The mesenteric arteries of hypertensive rats with bilaterally constricted renal arteries were observed by light, scanning electron and transmission electron microscopy. In the early stage of hypertensive arterial lesions, many leukocytes adhered to the endothelial surface, and large or small and polygonal endothelial cells were irregularly arranged. Sporadically brightened and atrophied endothelial cells were distributed on the injured surface. These atrophied cells were transmission electron microscopically confirmed to have undergone coagulation necrosis. In the surrounding of the atrophied cells were observed opened endothelial cell junctions and enlarged intercellular spaces to which many leukocytes and platelets adhered. Because of loosening of connection with neighboring cells, atrophied endothelial cells became solitary or being denuded. Opened endothelial cell junctions were also observed between the uninjured endothelial cells as well as in areas penetrated by leukocytic pseudopods. Where light microscopy disclosed the deposition of a large amount of fibrinoid substance in the intima and media, scanning electron microscopy showed opened endothelial cell junctions and denudation of endothelial cells. From the results of the present experimental study, it was suggested that in the genesis of the hypertensive rat arterial lesions, the degeneration, necrosis and denudation of endothelial cells, opened endothelial cell junctions between these cells, and insudation of blood plasma through the opened junctions or denuded areas might play important roles.

Animals↗