Schwartz S M
University of Washington/Department of Pathology, Seattle 98195-7335, USA.
Z Kardiol. 1995;84 Suppl 4:129-35.
Vascular narrowing, the clinical dilatation of narrowed vessels, and the restenosis of those vessels are central topics in modern cardiology. This review discusses the cellular basis both for the spontaneous narrowing of vessels and for the restenotic process that occurs after angioplasty. The central issue, as discussed in this review, is likely to be remodeling of the vessel wall rather than simple accretion of lipid mass in atherosclerosis or simple physical dilatation following angioplasty. While it is true that the atherosclerotic lesion grows by accretion of lipid mass, this by itself does not narrow vessels. As we will discuss, the vessel has a phenomenal ability to accommodate changes of this sort. Narrowing must occur, at least in part, because of a failure of this normal ability to accommodate. In a similar manner, one might expect the restonotic vessel to simply remodel itself down to its preangioplasty size. The issue for cell and molecular biologists is what "remodeling" means. Until recently, the assertion has been that remodeling occurred as the result of the formation of new intimal mass; that is, the atherosclerotic vessel was seen as returning to its original dimensions following angioplasty as a result of forming a new intimal mass that filled in the dilated space. Recent studies using cell kinetic methods as well as intravascular ultrasound, however, have cast doubt upon this hypothesis. It now appears that the loss of gain following angioplasty is likely to be due to the formation of new tissues which remodel the vessel wall without necessarily adding mass to it. This is the same sort of process that is well described in wound healing. The nature of this new tissue is of great interest. Studies in this laboratory and others have identified genes which may be unique to this tissue and explain the remodeling response.
血管狭窄、狭窄血管的临床扩张以及这些血管的再狭窄是现代心脏病学的核心课题。本综述讨论了血管自发狭窄以及血管成形术后再狭窄过程的细胞基础。如本综述所讨论的，核心问题可能是血管壁的重塑，而非动脉粥样硬化中脂质块的简单堆积或血管成形术后的单纯物理扩张。诚然，动脉粥样硬化病变是通过脂质块的堆积而生长，但这本身并不会使血管变窄。正如我们将讨论的，血管具有非凡的能力来适应这种变化。血管变窄至少部分是由于这种正常适应能力的失效。以类似的方式，人们可能期望再狭窄的血管简单地重塑自身回到血管成形术前的大小。细胞和分子生物学家面临的问题是“重塑”意味着什么。直到最近，一种观点认为重塑是新内膜形成的结果；也就是说，动脉粥样硬化血管在血管成形术后被视为通过形成填充扩张空间的新内膜而恢复到其原始尺寸。然而，最近使用细胞动力学方法以及血管内超声的研究对这一假设提出了质疑。现在看来，血管成形术后的再狭窄很可能是由于新组织的形成，这些新组织重塑了血管壁，但不一定增加了其质量。这与伤口愈合中描述得很清楚的过程是同一类。这种新组织的性质非常有趣。本实验室和其他实验室的研究已经鉴定出可能是这种组织特有的基因，并解释了重塑反应。
