Faculty Bibliography

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 intimal 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.(ABSTRACT TRUNCATED AT 250 WORDS)

BACKGROUND. Basic fibroblast growth factor (bFGF) is a potent local promoter of vascular smooth muscle cell migration and proliferation and may play a major role in the pathogenesis of intimal fibromuscular lesions. Preliminary studies have shown that exogenous bFGF localizes to injured rabbit aorta and suggest that this interaction might be inhibited by anti-bFGF immunoglobulin (Ig) G. This study was designed to evaluate the possible role of polyclonal anti-bFGF IgG in reducing intimal fibromuscular lesion formation in the injured rabbit aorta. METHODS. The abdominal aortic endothelium was subjected to balloon injury in 13 rabbits. Six rabbits received intravenous rabbit anti-bFGF IgG, and seven received irrelevant rabbit IgG (16 micrograms/kg) 30 minutes before injury and daily for 5 days after injury. At 14 days after injury the aorta was fixed and sectioned, and the intimal and medial areas were measured by computerized digital morphometry with the intimal/medial ratio as an index of neointimal lesion formation. RESULTS. In the control group the intimal/medial ratio was 0.538 +/- 0.046 (mean +/- SEM), which was significantly greater than the anti-bFGF-treated group value of 0.148 +/- 0.021 (p < 0.001). CONCLUSIONS. These results show that daily doses of intravenous polyclonal anti-bFGF IgG for 5 days after balloon aortic injury significantly inhibit intimal fibromuscular lesion formation at 14 days. The results suggest that the process of intimal fibromuscular lesion formation may be susceptible to modification by antagonists to bFGF

Sterol 27-hydroxylase activity in bovine aortic endothelial (BAE) cells in culture has been compared with that in HepG2 cells and in Chinese hamster ovary (CHO) cells using identical culture conditions. The total enzyme activity of BAE cells (3.0 nmol/72 h per mg cell protein) was comparable with that of HepG2 cells (4.0 nmol/72 h per mg protein) and both values were significantly greater than that in CHO cells (0.002 nmol/72 h per mg protein). The enzyme was identified in the mitochondria extracted from BAE cells by Western blotting using an antibody of proven specificity, and its metabolites 27-hydroxycholesterol and 3 beta-hydroxy-5-cholestenoic acid were identified by mass spectrum analysis. The presence of the enzyme in endothelium provides a mechanism for preventing accumulation of intracellular cholesterol by initiating a pathway of bile acid synthesis different from that initiated by 7 alpha-hydroxylation of cholesterol in the liver

Imaging evaluation is important in the follow-up of patients who have undergone surgical repair of the aorta. We present a case in which MR imaging demonstrated compression of the superior vena cava (SVC) as a late complication of ascending aortic aneurysm surgery. This complication led to thrombosis and clinical SVC syndrome