SUPPRESSION OF NEOINTIMAL LESIONS AFTER VASCULAR INJURY - A ROLE FOR POLYCLONAL ANTI-BASIC FIBROBLAST GROWTH-FACTOR ANTIBODY

Citation
Hc. Nguyen et al., SUPPRESSION OF NEOINTIMAL LESIONS AFTER VASCULAR INJURY - A ROLE FOR POLYCLONAL ANTI-BASIC FIBROBLAST GROWTH-FACTOR ANTIBODY, Surgery, 116(2), 1994, pp. 456-462
Citations number
25
Categorie Soggetti
Surgery
Journal title
ISSN journal
00396060
Volume
116
Issue
2
Year of publication
1994
Pages
456 - 462
Database
ISI
SICI code
0039-6060(1994)116:2<456:SONLAV>2.0.ZU;2-1
Abstract
Background. Basic fibroblast growth factor (bFGF) is a potent local pr omoter of vascular smooth muscle cell migration and proliferation and may play a major role in the pathogenesis of intimal fibromuscular les ions. Preliminary studies have shown that exogenous bFGF localizes to injured rabbit aorta and suggest that this interaction might be inhibi ted by anti-bFGF immunoglobulin (Ig) G. This study was designed to eva luate the possible role of polyclonal anti-bFGF IgG in reducing intima l fibromuscular lesion formation in the injured rabbit aorta. Methods. The abdominal aortic endothelium was subjected to balloon injury in 1 3 rabbits. Six rabbits received intravenous rabbit anti-bFGF IgG, and seven received irrelevant rabbit IgG (16 mu g/kg) 30 minutes before in jury and daily for 5 days after injury. At 14 days after injury the ao rta was fixed and sectioned, and the intimal and medial areas were mea sured by computerized digital morphometry with the intimal/medial rati o as an index of neointimal lesion formation. Results. In the control group the intimal/medial ratio was 0.538 +/- 0.046 (mean +/- SEM), whi ch was significantly greater than anti-bFGF-treated group value of 0.1 48 +/- 0.021 (p < 0.001). Conclusions. These results show that daily d oses of intravenous polyclonal anti-bFGF IgG for 5 days after balloon aortic injury significantly inhibit intimal fibromuscular lesion forma tion at 14 days. The results suggest that the process of intimal fibro muscular lesion formation may be susceptible to modification by antago nists to bFGF.