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Ann Thorac Surg 1994;58:308-311
© 1994 The Society of Thoracic Surgeons
Division of Cardtothoracic Surgery, Departments of Surgery and Cell Biology, New York University Medical Center, New York, New York USA
* Address reprint requests to Dr Grossi, Division of Cardiovascular Surgery. New York University Medical Conter, 530 First Ave, Ste 6-D, New York, NY 10016.
Neointimal hyperplasia limits the long-term patency of saphenous vein grafts (SVGs), but is notably absent from most internal mammary artery (IMA) grafts. Basic fibroblast growth factor (bFGF) is a local endothelial and vascular smooth muscle mitogen known to be involved in the pathogenesis of neointimal hyperplasia. This study used an animal model to compare the number of available high-affinity (HAR) and low-affinity (LAR) bFGF receptors in SVGs and IMA grafts and to determine whether distention injury causes an increase in receptor availability. The IMA and SVG specimens were harvested from 12 dogs and distended at 25 or 200 mm Hg for 15 minutes, and then the bFGF receptor uptake was measured in them using iodine 125-labeled bFGF. In the IMA conduits distended at low pressure, there were 2.54 ± 0.10 (mean ± standard error of the mean) HARs per mm2 of intimai surface area available and 5.19 ± 0.40 LARs per mm2. High-pressure distention significantly (p < 0.001) increased the number of available HARs to 5.06 ± 0.27 per mm2 and of LARs to 7.27 ± 0.042 per mm2. At low pressure, the SVGs had significantly (p < 0.001) more HARs (9.14 ± 0.84 per mm2) and LARs (18.2 ± 0.57 per mm2) available than did the IMA conduits, and high pressure significantly (p < 0.001) increased the number of HARs available in SVGs to 24.1 ± 2.43 per mm2 and the number of LARs to 44.7 ± 2.34 per mm2. These results demonstrate that there is a significantly higher number of available bFGF receptors per unit of surface area in dog SVGs than IMA grafts. High-pressure distention further increases the differences in the number of available bFGF receptors between SVGs and IMA grafts (p < 0.001). These findings suggest a newly recognized mechanism that may contribute to the increased intimai hyperplasia found in implanted SVGs but not IMAs.
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