Role of Blood-borne Cells in Organization of Mural Thrombi

Ghani, Abdul Rahman Izaini; Tibbs, David J.

doi:10.1136/bmj.1.5287.1244

Cited by 43 publications

(9 citation statements)

References 4 publications

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“…However, Poole, Sanders, and Florey (1958) reported that intimal lesions in the rabbit aorta were still not completely healed after 33 weeks. The two principal suggestions as to the origin of the new endothelial cells are (a) the intimal surface is restored by growth of the undamaged endothelial cells at the edges of the lesion, spreading into and covering the denuded area (Poole, Sanders, and Florey, 1959), and (b) the continuity of the luminal cells is restored by circulating mononuclear cells (Ghani and Tibbs, 1962). Alternative propositions are based on the fact that these early lining cells closely resemble macrophages (Buck, 1961) or smooth-muscle cells (Nomura, 1970).…”

Section: Discussionmentioning

confidence: 99%

The histopathology of small vessels following microvascular repair

Baxter

O’Brien

Henderson

et al. 1972

Journal of British Surgery

142

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1. The histopathological findings following microvascular repair of 105 arteries and 89 veins in Englishstrain rabbits are reported. 2. The importance of (a) the accurate apposition of the vessel walls and (b) the avoidance of excesive medial necrosis is stressed. 3. The process of subintimal hyperplasia is described and the importance of its role in the repair of small vessels is discussed. Previously, the new formation of elastin tissue has been considered pathognomonic of vascular disease. 4. The appreciably slower rate of repair in veins is also reported. 5. From these observations suggestions have been made with regard to improved technique of surgical repair.

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Section: Discussionmentioning

confidence: 99%

The histopathology of small vessels following microvascular repair

Baxter

O’Brien

Henderson

et al. 1972

Journal of British Surgery

142

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“…These observations suggest a diffuse repopulation rather than one derived by direct proliferation from local foci. (2) The diffuse repopulation could have represented colonization onto the denuded areas by circulating blood cells; this type of healing has been suggested by other investigators (5,10,11). Participation of such circulating cells is rendered less likely by the failure of killed grafts to indicate any colonization response.…”

Section: Discussionmentioning

confidence: 82%

Intimal injury and regrowth in the rabbit aorta; medial smooth muscle cells as a source of neointima.

Spaet¹,

Stemerman²,

Veith³

et al. 1975

Circulation Research

152

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The present study was undertaken to determine the mechanism of neointima formation in rabbit arteries subjected to extensive endothelial desquamation. Endothelial cells were selectively removed from the abdominal aorta by passing an inflated balloon catheter through the vessel. The healing response was then studied serially for up to a week, when neointima formation had provided a virtually complete cover. In en face preparations, the early neointimal cells appeared in random locations; they did not develop in apposition to residual, healthy endothelium. The possibility of blood cell colonization was explored by inserting killed aortic homografts. Since these homografts showed neointima formation only close to the site of junction with the normal aorta and as a direct extension of healthy endothelium, the likelihood of significant blood cell colonization was deemed small. Histologic and electron microscopic sections provided evidence that the early neointimal cells in the healing aorta were derived from medial smooth muscle cells. Healing of the injured arterial intima was accompanied by thickening instead of prompt restoration to normal, and the thickened intima resembled an arteriosclerotic plaque. The present study thus supports the concept that arteriosclerosis is a disease involving proliferation of medial smooth muscle cells. KEY WORDS intimal thickening deendothelialization artery healing experimental arteriosclerosis intimal balloon injury vessel trauma• The normal blood vessel intima appears to represent a remarkably stable tissue because it demonstrates an extremely low rate of cell turnover (1-3 58associates (4) have concluded from studies on mechanically traumatized rabbit aortas that such a direct extension of endothelium is the source of the new cover and that many weeks are required for most areas of damage to become reendothelialized.In the present study endothelium was selectively stripped from rabbit aortas by a balloon catheter technique. Arterial intimas that had been devoid of endothelial cells at the lumen immediately following this procedure were found to be completely covered by a fresh layer of cells after 1 week; we called this new cover the neointima. Three possible sources of the new intimal cells at this early healing phase were considered; (a) proliferative extension of endothelium from undamaged areas as reported in earlier studies (4), (b) colonization of the denuded areas by circulating blood cells that subsequently undergo transformation (5), and (c) migration, metamorphosis, and proliferation of medial smooth muscle cells. Our present data indicated that the major source of early neointima in the experimental situation studied was smooth muscle cells from the media, a possibility first suggested in 1936 by Stchelkounoff (6).

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“…Whether the origin of neoendothelium on implanted vascular prostheses is in circulating blood cells has been investigated. [11][12][13][14] However, this hypothesis has not been widely accepted because it was not recognized that circulating blood cells contained progenitor endothelial cells. In 1997, Asahara et al 28 mentioned that the peripheral blood contained certain cells that can differentiate into endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

“…[8][9][10] Furthermore, some researchers have reported that endothelia were derived from cells in circulating blood. [11][12][13][14] Recently, progenitor endothelial cells in circulating blood were reported; these progenitor endothelial cells participated in neoendothelialization on the vascular graft surface. However, it was not shown how these progenitor endothelial cells ultrastructually differentiated into neoendothelia.…”

Section: Introductionmentioning

confidence: 99%

Progenitor endothelial cells on vascular grafts: An ultrastructural study

Maeda

Fukui

Nakamura

et al. 2000

J. Biomed. Mater. Res.

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The morphology of progenitor endothelial cells on vascular graft surfaces is addressed in this report. Such cells were seen to attach to intima-expressed CD34 and Flk-1 antigen and showed positive 5-bromo-2-deoxyuridine (BrdU) uptake. We examined CD34 and Flk-1 antigen-expressing endothelial progenitor cells three-dimensionally using confocal laser scanning microscopy (CLSM). Under detailed CLSM observation, through an ameboid-form cell, these progenitor endothelial cells changed from a globular to a flattened form. We also investigated these morphological changes using scanning electron microscopy. From these results, progenitor endothelial cells were observed not only near the advancing edge of endothelium, but also around the developing intimal site. Their form also changed from globular to flattened as observed in the CLSM results. These morphological changes were seen more frequently near the advancing edge and around the developing intimal site. They attached directly to vascular prosthesis fibers and likewise covered the graft luminal surface. Progenitor endothelial cells in any form had a common surface structure. We conclude from our results that progenitor endothelial cells can attach to graft fibers directly without clotting and directly cover the graft luminal surfaces.

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Role of Blood-borne Cells in Organization of Mural Thrombi

Cited by 43 publications

References 4 publications

The histopathology of small vessels following microvascular repair

The histopathology of small vessels following microvascular repair

Intimal injury and regrowth in the rabbit aorta; medial smooth muscle cells as a source of neointima.

Progenitor endothelial cells on vascular grafts: An ultrastructural study

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