| Autor: |
J.M. Reiner, Florentin Fa, W.M. Lee, Wilbur A. Thomas, Kyu Taik Lee |
| Rok vydání: |
1976 |
| Předmět: |
|
| Zdroj: |
Experimental and Molecular Pathology. 24:360-374 |
| ISSN: |
0014-4800 |
| DOI: |
10.1016/0014-4800(76)90071-x |
| Popis: |
The sine qua non of the lesion of atherosclerosis in man and experimental animals is excessive focal accumulation of modified smooth muscle cells in the intima of arteries. In advanced stages extensive necrosis with accumulation of lipid-rich debris is a prominent feature. In swine fed hypercholesterolemic (HC) diets focal atherosclerotic lesions are produced, but they progress slowly and do not develop frank necrosis until they have been on HC diet for many months or even years. The atherosclerotic process can be greatly accelerated by traumatizing the arterial intima with a ballon-catheter in addition to feeding the HC diet. Within a few months thick atherosclerotic lesions with extensive necrosis and calcification can be produced. In regard to arterial cell population dynamics, we showed in the first part of the current study that under the specified experimental conditions, lesions produced in young swine by balloon-catheter trauma and HC diet have at least four features in common with lesions produced in young swine by HC diet alone. (1) Multiple cells are involved in the initiation of the lesions (i.e., they are not monoclonal in origin). (2) The cells do not divide in a completely random fashion. (3) The division pattern is consistent with polyclonal origin with considerable heterogeneity as regards growth rate. (4) Most and perhaps all lesion cells were in the dividing population during the periods that were studied. The differences observed between development of lesions produced by HC diet alone and those produced by HC diet plus ballon-catheter intimal trauma were quantitative and not qualitative, i.e., the lesions produced by the latter procedure had a greater rate of cell multiplication and proceeded more rapidly to the necrotic stage than did those produced by HC diet alone. In the second part of the current study, we have devised a method for calculating cell deaths in the atherosclerotic lesions produced by HC diet plus intimal trauma. In the period 60–97 days on HC diet which was studied we found that circa 40% of the lesion cells died during the perireplicative and/or perimitotic period of the cell cycle. The high cell death rate was offset in part by a high cell birth rate. As indicated by tritiated thymidine ( 3 HTdR) labeling indices, approximately four times as many cells were synthesizing DNA at the time of observation as in the adjacent normal appearing media. Obviously the rate of growth of the atherosclerotic lesions that were studied was determined by the balance between excessive cell birth and death rates. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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