EXPERIMENTAL ARTERIOSCLEROSIS

EXPERIMENTAL ARTERIOSCLEROSIS
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实验性动脉硬化

DOI:
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发表时间:
1972
影响因子:
15.3
通讯作者:
R. Ross
R. Ross
中科院分区:
医学1区
文献类型:
--
作者:
M. Stemerman;R. Ross

文献摘要

被引文献

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通过用动脉内球囊导管选择性去除血管内皮,在猴(Macaca nemestrina)中产生动脉炎性病变。去内皮化后,血小板层立即覆盖裸露区域。血栓逐渐被清除,7天后,血管似乎大部分重新内皮化。从第4天开始,平滑肌细胞经历修饰并通过内弹性膜中的窗孔迁移到内膜中,在内膜中它们增殖。到28天时,内膜病变由多层平滑肌细胞组成,周围有胶原和弹性纤维以及基底样物质。3个月后,病变明显增生,并含有新的细胞外结缔组织成分。相比之下,6个月后没有进一步损伤,病变大小显著减小,表明在没有持续内皮损伤的情况下,病变可能是可逆的。内皮“损伤”的重要性使中膜平滑肌暴露于血浆成分,这可能是与平滑肌细胞迁移和增殖进入内膜导致病变相关的主要因素。平滑肌细胞不含脂质。这种病变的相似之处,纤维肌肉弹性病变或动脉粥样硬化前内膜增生的人,使其成为一个有用的模型,为进一步研究动脉粥样硬化。
Arteriosclerotic lesions have been produced in monkeys (Macaca nemestrina) by selective removal of the vascular endothelium with an intra-arterial balloon catheter. Immediately after de-endothelialization a platelet layer covers the denuded area. This thrombus is gradually removed and by 7 days the vessel appears to be largely reendothelialized. Beginning at day 4, smooth muscle cells undergo modification and migrate through fenestrae in the internal elastic lamina into the intima where they proliferate. By 28 days, the intimal lesion consists of multiple layers of smooth muscle cells surrounded by collagen and elastic fibers and basement-like material. After 3 months the lesions are markedly hyperplastic and contain new extracellular connective tissue elements. In contrast, with no further injury after 6 months the lesion has decreased markedly in size suggesting that it may be reversible in the absence of continued endothelial injury. The importance of endothelial "injury" exposing medial smooth muscle to plasma constituents may be the principal factors associated with the migration and proliferation of the smooth muscle cells into the intima resulting in the lesion. The smooth muscle cells do not contain lipid. The similarities of this lesion to the fibromusculo-elastic lesion or preatherosclerotic intimal hyperplasia in man makes it a useful model for the further study of atherosclerosis.