Folgen des Gefäßkatheterismus am normo- und hypercholesterinaemischen Kaninchen

Baumgartner, Hans R.; Studer, Amy

doi:10.1159/000161922

Cited by 38 publications

(10 citation statements)

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“…A second consideration may be of additional major importance. The present study and those of other investigators (14,16) have shown that the healing neointima undergoes progressive thickening over a period of months, leading to the formation of a lesion resembling the arteriosclerotic plaque. When the vascular insult is not repeated or continued, there is ultimate regression, so that about 6 months after injury, the thickness of the intima is restored virtually to normal (14,17).…”

Section: Figuresupporting

confidence: 78%

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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Section: Figuresupporting

confidence: 78%

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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“…A long standing hypothesis of atherosclerosis (17) which has recently received considerable attention is that endothelial injury initiates a series of steps that leads to medial smooth muscle cell migration and proliferation (2,15,16,(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28) characteristic of the arteriosclerotic lesions. Several variations of the endothelial injury hypothesis have been a topic of intensive study in our laboratory (21,22,29) and those of others (30)(31)(32)(33)(34).…”

Section: Discussionmentioning

confidence: 99%

The effect of thrombocytopenia on experimental arteriosclerotic lesion formation in rabbits. Smooth muscle cell proliferation and re-endothelialization.

Friedman¹,

Stemerman²,

Wenz³

et al. 1977

J. Clin. Invest.

291

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A B S T R A C T This study was designed to investigate the mechanisms involved in fibromusculoelastic lesion formation produced by selective de-endothelialization by the intra-arterial balloon catheter technique in thrombocytopenic rabbits. Thrombocytopenia was induced and maintained for up to 31 days by daily injections of highly specific sheep anti-rabbit platelet sera (APS). Evidence for re-endothelialization was obtained by i.v. Evans blue dye 30 min before sacrifice. Rabbits received daily injections of APS, which reduced the mean platelet count to 5,600/cm3; control animals received identically treated normal sheep sera on the same schedule, and had mean daily platelet counts of 363,000/cm3. Evaluation of intimal thickness was assessed by counting cell layers in semithin sections. Intimal thickening in aortae from rabbits treated with APS was strikingly suppressed, in contrast to those from normal sheep sera-treated animals which showed a mean intimal thickness of 18 cell layers within 28 days often after de-endothelialization. Re-endothelialization was not affected by APS treatment. These results indicate that the proliferation of smooth muscle cells which is characteristic ofarteriosclerotic lesions is dramatically inhibited by reduction of platelets.

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“…Rats were preanesthetized with enflurane (Ethrane, Abbott Laboratories) for 60 seconds and anesthetized with pentobarbital sodium (Nembutal sodium, Abbott, 35 mg/kg body wt IP), and the endothelium of the thoracic aorta was removed by the method of Baumgartner and Studer, 14 with minor modifications. 3 To verify the degree of aortic denudation, six rats randomly selected received 1 mL IV of Evans blue (Merck; 1% solution in 0.9% NaCl) immediately after the catheter-induced lesion and were killed 30 minutes later by cervical dislocation.…”

Section: Methods Animalsmentioning

confidence: 99%

Rat aortic smooth muscle cells isolated from different layers and at different times after endothelial denudation show distinct biological features in vitro.

Orlandi

Ehrlich

Ropraz

et al. 1994

Arterioscler Thromb

102

105

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Endothelial denudation by balloon injury of the rat aorta induces the development of a neointima as a consequence of the migration and proliferation of smooth muscle cells (SMCs). Initially, intimal SMCs show a dedifferentiated phenotype, which reverts to a normal differentiated phenotype after endothelial cells have resurfaced the vessel lumen. We investigated in vitro the proliferative and phenotypic features of SMCs from different layers of rat aorta isolated 15 and 60 days after endothelial denudation. Freshly isolated intimal cells 15 days after balloon injury (IT-15) appeared rounded and showed a decreased content of a-smooth muscle actin, smooth muscle myosin, and desmin compared with intimal cells isolated 60 days after balloon injury . No morphological and cytoskeletal differences were observed among freshly isolated IT-60 cells and other medial populations, which included medial SMCs that underlie the intimal thickening. In culture, IT-15 cells showed increased proliferative activity both in monolayers and in free-floating collagen lattices. Decreased expression of a-smooth muscle actin and I ntimal thickening after endothelial denudation has been widely used as a model for the development of the atheromatous plaque and has furnished useful information on smooth muscle cell (SMC) susceptibility to microenvironmental stimuli. 16 Only a small proportion of medial SMCs are activated to migrate and replicate after endothelial denudation 5 ; this may reflect a heterogeneity of SMC phenotypic features that has been described by means of several other criteria. 6 " It has been shown that cultured SMCs from the normal media and from the experimental intimal thickening show different growth patterns. SMCs from the intimal thickening, collected 15 days after endothelial lesion, proliferate more actively than do medial cells in the presence of the same amounts of serum; moreover, contrary to medial cells, SMCs are capable of growing in the absence of serum factors. 48This behavior is also seen in normal medial SMCs Received December 17, 1993; revision accepted February 11, 1994.From the Department of Pathology, University of Geneva, Switzerland (A.O., H.P.E., P.R., G.G.); the Department of Pathology, University "Tor Vergata" of Rome, Italy (A.O., L.G.S.); and the Department of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston (H.P.E.).Reprint requests to Dr Giulio Gabbiani, Department of Pathology, University of Geneva, CMU-1, rue Michel-Servet, CH-1211 Geneva 4, Switzerland. smooth muscle myosin was documented in IT-15 cells compared with IT-60 cells and other medial SMC populations in monolayer. Moreover, IT-15 cells suspended in collagen lattices were poor at contracting these collagen lattices compared with IT-60 and control SMCs. IT-60 cells were equivalent to control SMCs at lattice contraction except for a temporary delay at day 1. Cells from the media underlying the intimal thickening isolated 15 and 60 days after balloon injury proliferated less, had an increased content...

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Folgen des Gefäßkatheterismus am normo- und hypercholesterinaemischen Kaninchen

Cited by 38 publications

References 0 publications

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

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

The effect of thrombocytopenia on experimental arteriosclerotic lesion formation in rabbits. Smooth muscle cell proliferation and re-endothelialization.

Rat aortic smooth muscle cells isolated from different layers and at different times after endothelial denudation show distinct biological features in vitro.

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