Kleinert L B, Hoying J B, Williams S K
Department of Surgery, University of Arizona, Tucson 85724, USA.
Cell Transplant. 1996 Jul-Aug;5(4):475-82. doi: 10.1177/096368979600500406.
Endothelial cell transplantation onto polymeric vascular grafts results in the formation of a neointima. The formation of this neointima is often suggested to result from a chronic cellular hyperplasia where the terms intimal hyperplasia and intimal thickening are used interchangeably. While the formation of a midgraft neointima in sodded grafts involves a level of cell proliferation, the synthesis and deposition of extracellular matrix proteins is also a ubiquitous observation in these grafts. To assess the composition of midgraft neointima in sodded grafts, a morphometric method was developed to provide a differential quantitation of the cellular-hyperplastic and extracellular-hypertrophic elements of intimal thickening. The formed neointima on microvessel endothelial cell sodded and control (noncell-treated) ePTFE vascular grafts was quantified after 3, 12, and 52 wk of graft implantation in a canine carotid artery model. Midgraft sections of grafts were evaluated for both intimal thickness (IT) and cell density per unit volume and quantified using a PC-based image analysis program. Sodded grafts explanted at 3 wk exhibited an average neointimal cell density (3 x 10(9) cells/cm3; IT 30 microns) equivalent to cell densities observed in normal arterial media. After 12 wk the mean cell density approached a hyperplastic value (3.7 x 10(9) cells/cm3; IT 76 microns), while grafts explanted after 52 wk exhibited a mean cell density (2.8 x 10(9) cells/cm3; IT 30 microns) similar to 3-wk values. Control grafts that received no cells exhibited no midgraft cellular coverage. These results indicate that neointima formation in the midgraft region of sodded grafts occurred via mechanisms involving both a cellular hyperplasia and an extracellular hypertrophy. Differential responses occur presumably due to localized differences in cellular proliferation and cellular biosynthetic activity.
将内皮细胞移植到聚合物血管移植物上会导致新内膜的形成。这种新内膜的形成通常被认为是慢性细胞增生的结果，其中内膜增生和内膜增厚这两个术语可以互换使用。虽然在植皮移植物中中移植物新内膜的形成涉及一定程度的细胞增殖，但细胞外基质蛋白的合成和沉积在这些移植物中也是普遍存在的现象。为了评估植皮移植物中移植物新内膜的组成，开发了一种形态计量学方法，以对内膜增厚的细胞增生和细胞外肥大成分进行差异定量。在犬颈动脉模型中，将微血管内皮细胞植皮和对照（未处理细胞）的ePTFE血管移植物植入3、12和52周后，对形成的新内膜进行定量。对移植物的中移植物切片进行内膜厚度（IT）和单位体积细胞密度评估，并使用基于PC的图像分析程序进行定量。在3周时取出的植皮移植物显示平均新内膜细胞密度（3×10⁹个细胞/cm³；IT 30微米），与正常动脉中膜中观察到的细胞密度相当。12周后，平均细胞密度接近增生值（3.7×10⁹个细胞/cm³；IT 76微米），而52周后取出的移植物显示平均细胞密度（2.8×10⁹个细胞/cm³；IT 30微米）与3周时的值相似。未接受细胞的对照移植物没有中移植物细胞覆盖。这些结果表明，植皮移植物中移植物区域的新内膜形成是通过涉及细胞增生和细胞外肥大的机制发生的。推测不同的反应是由于细胞增殖和细胞生物合成活性的局部差异所致。
