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
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兔主动脉内膜损伤和再生:内侧平滑肌细胞作为新内膜的来源

DOI:
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发表时间:
1975
影响因子:
20.1
通讯作者:
I. Lejnieks
I. Lejnieks
中科院分区:
医学1区
文献类型:
--
作者:
T. Spaet;M. Stemerman;F. Veith;I. Lejnieks

文献摘要

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本研究旨在确定兔动脉广泛内皮剥脱后新生内膜形成的机制。通过使膨胀的球囊导管穿过血管选择性地从腹主动脉移除内皮细胞。然后连续研究愈合反应长达一周,此时新生内膜形成提供了几乎完全的覆盖。在表面制备中,早期新生内膜细胞出现在随机位置;它们不与残留的健康内皮贴壁发育。血细胞定植的可能性通过插入灭活的同种主动脉来探索。由于这些同种移植物仅在与正常主动脉连接部位附近显示新生内膜形成,并且是健康内皮的直接延伸,因此认为显著血细胞定植的可能性很小。组织学和电子显微镜切片提供的证据表明,愈合的主动脉中的早期新生内膜细胞来自中膜平滑肌细胞。损伤动脉内膜的愈合伴随着增厚,而不是迅速恢复正常,增厚的内膜类似于动脉斑块。因此,本研究支持动脉硬化是一种涉及中膜平滑肌细胞增殖的疾病的概念。
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.