Ultrastructural elements in experimental intimal thickening. I. Electron microscopic study of the development and cellular elements of intimal proliferation

B. Veress, A. Kádár, H. Jellinek

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Abstract

The development of intimal thickening in the rat aorta was follwed up in model experiments and the ultrastructure of its cell components was studied. The surface of the proliferation was covered by endothelial cells, the majority of which had obviously crept there from the intact part of the aortic wall. In a lesser degree also the blood's cellular elements appeared to participate in the formation of the endothelial cell row. The multilayered proliferation which had developed between the row of endothelial cells and the damaged internal elastic lamina consisted exclusively of smooth muscle cells; at least we failed to identify any other cell type within it. In the smooth muscle cells of aged proliferation, degeneration was signified by the presence of myelin figures. Neutral fat droplets appeared also in the extracellular space, having apparently passed through the endothelium from the blood plasma to the thickening. It seems, therefore, that there is no notable morphological difference between the intimal thickening serving as experimental model and the early arteriosclerotic lesion and accordingly a closer study of regenerative intimal proliferation may contribute some new information on the pathomechanism of degenerative and regenerative processes taking place in the vessel wall.

Original languageEnglish
Pages (from-to)200-211
Number of pages12
JournalExperimental and Molecular Pathology
Volume11
Issue number2
Publication statusPublished - Oct 1969

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Tunica Intima
Endothelial cells
Endothelial Cells
Electrons
Smooth Muscle Myocytes
Muscle
Blood
Cells
Extracellular Space
Cellular Structures
Myelin Sheath
Endothelium
Aorta
Rats
Creep
Theoretical Models
Fats
Cell Proliferation
Plasmas
Experiments

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Molecular Biology
  • Clinical Biochemistry

Cite this

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abstract = "The development of intimal thickening in the rat aorta was follwed up in model experiments and the ultrastructure of its cell components was studied. The surface of the proliferation was covered by endothelial cells, the majority of which had obviously crept there from the intact part of the aortic wall. In a lesser degree also the blood's cellular elements appeared to participate in the formation of the endothelial cell row. The multilayered proliferation which had developed between the row of endothelial cells and the damaged internal elastic lamina consisted exclusively of smooth muscle cells; at least we failed to identify any other cell type within it. In the smooth muscle cells of aged proliferation, degeneration was signified by the presence of myelin figures. Neutral fat droplets appeared also in the extracellular space, having apparently passed through the endothelium from the blood plasma to the thickening. It seems, therefore, that there is no notable morphological difference between the intimal thickening serving as experimental model and the early arteriosclerotic lesion and accordingly a closer study of regenerative intimal proliferation may contribute some new information on the pathomechanism of degenerative and regenerative processes taking place in the vessel wall.",
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AU - Veress, B.

AU - Kádár, A.

AU - Jellinek, H.

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N2 - The development of intimal thickening in the rat aorta was follwed up in model experiments and the ultrastructure of its cell components was studied. The surface of the proliferation was covered by endothelial cells, the majority of which had obviously crept there from the intact part of the aortic wall. In a lesser degree also the blood's cellular elements appeared to participate in the formation of the endothelial cell row. The multilayered proliferation which had developed between the row of endothelial cells and the damaged internal elastic lamina consisted exclusively of smooth muscle cells; at least we failed to identify any other cell type within it. In the smooth muscle cells of aged proliferation, degeneration was signified by the presence of myelin figures. Neutral fat droplets appeared also in the extracellular space, having apparently passed through the endothelium from the blood plasma to the thickening. It seems, therefore, that there is no notable morphological difference between the intimal thickening serving as experimental model and the early arteriosclerotic lesion and accordingly a closer study of regenerative intimal proliferation may contribute some new information on the pathomechanism of degenerative and regenerative processes taking place in the vessel wall.

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