Dipyridamole directly inhibits vascular smooth muscle cell proliferation in vitro and in vivo: Implications in the treatment of restenosis after angioplasty

Singh, Jai Pal; Rothfuss, Kimberly J.; Wiernicki, Todd R.; Lacefield, William B.; Kurtz, Leon E.; Brown, Raymond F.; Brune, K; Bailey, Dianna L.; Dubé, Gregory P.

doi:10.1016/0735-1097(94)90752-8

Cited by 50 publications

(21 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The non-thrombogenicity and the antiproliferative ability are dependent on the DPA dose according to a previous report [23]. DPA was locally delivered into a rabbit model with carotid or femoral artery injury, and exhibited a dose-dependent inhibition of SMC proliferation [21]. In this study, the dose dependence was not distinct in non-thrombogenicity, whereas it was shown in HASMC proliferation inhibition.…”

Section: Discussionmentioning

confidence: 61%

Electrospun biodegradable elastic polyurethane scaffolds with dipyridamole release for small diameter vascular grafts

et al. 2014

View full text Add to dashboard Cite

Acellular biodegradable small diameter vascular grafts (SDVGs) require antithrombosis, intimal hyperplasia inhibition and rapid endothelialization to improve the graft patency. However, current antithrombosis and antiproliferation approaches often conflict with endothelial cell layer formation on SDVGs. To address this limitation, biodegradable elastic polyurethane urea (BPU) and the drug dipyridamole (DPA) were mixed and then electrospun into a biodegradable fibrous scaffold. The BPU would provide the appropriate mechanical support, while the DPA in the scaffold would offer biofunctions as required above. We found that the resulting scaffolds had tensile strengths and strains comparable with human coronary artery. The DPA in the scaffolds was continuously released up to 91 days in phosphate buffer solution at 37 °C, with a low burst release within the first 3 days. Compared to BPU alone, improved non-thrombogenicity of the DPA-loaded BPU scaffolds was evidenced with extended human blood clotting time, lower TAT complex concentration, lower hemolysis and reduced human platelet deposition. The scaffolds with a higher DPA content (5 and 10%) inhibited proliferation of human aortic smooth muscle cell significantly. Furthermore, the DPA-loaded scaffolds had no adverse effect on human aortic endothelial cell growth, yet it improved their proliferation. The attractive mechanical properties and biofunctions of the DPA-loaded BPU scaffold indicate its potential as an acellular biodegradable SDVG for vascular replacement.

show abstract

Section: Discussionmentioning

confidence: 61%

Electrospun biodegradable elastic polyurethane scaffolds with dipyridamole release for small diameter vascular grafts

et al. 2014

View full text Add to dashboard Cite

show abstract

“…A number of drugs have been shown to inhibit the growth of vascular smooth muscle cells (e.g., heparin [18], calcium channel blockers [19], angiotensin-converting enzyme inhibitors [20], dipyridamole [21,22], and paclitaxel [11,12]). Attempts to reduce vascular stenosis in various animal models by the systemic administration of these agents have been largely unsuccessful.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of neointimal hyperplasia in vascular grafts by sustained perivascular delivery of paclitaxel

Masaki¹,

Rathi²,

Zentner³

et al. 2004

Kidney International

View full text Add to dashboard Cite

show abstract

“…A large multicenter trial sponsored by the National Institutes of Health using the oral combination of dipyridamole and aspirin in preventing AV graft failure in dialysis patients is ongoing. Continuous adventitial dipyridamole delivery using an osmotic pump inhibited NH formation in rabbit artery-injury models 202. In contrast, there was no significant decrease in restenosis rates after coronary angioplasty using intracoronary dipyridamole in a small randomized clinical trial 203.…”

Section: Prevention Strategiesmentioning

confidence: 99%

Neointimal hyperplasia associated with synthetic hemodialysis grafts

Terry

Shiu

et al. 2008

Kidney International

113

View full text Add to dashboard Cite

Stenosis is a major cause of failure of hemodialysis vascular grafts and is primarily caused by neointimal hyperplasia (NH) at the anastomoses. The objective of this article is to provide a scientific review of the biology underlying this disorder and a critical review of the state-of-the-art investigational preventive strategies in order to stimulate further research in this exciting area. The histology of the NH shows myofibroblasts (that are probably derived from adventitial fibroblasts), extracellular matrices, pro-inflammatory cells including foreign-body giant cells, a variety of growth factors and cytokines, and neovasculature. The contributing factors of the pathogenesis of NH include surgical trauma, bioincompatibility of the synthetic graft, and the various mechanical stresses that result from luminal hypertension and compliance mismatch between the vessel wall and graft. These mechanical stimuli are focal in nature and may have a significant influence on the preferential localization of the NH. Novel mechanical graft designs and local drug delivery strategies show promise in animal models in preventing graft NH development. Successful prevention of graft stenosis would provide a superior alternative to the native fistula as hemodialysis vascular access.

show abstract

Dipyridamole directly inhibits vascular smooth muscle cell proliferation in vitro and in vivo: Implications in the treatment of restenosis after angioplasty

Cited by 50 publications

References 20 publications

Electrospun biodegradable elastic polyurethane scaffolds with dipyridamole release for small diameter vascular grafts

Electrospun biodegradable elastic polyurethane scaffolds with dipyridamole release for small diameter vascular grafts

Inhibition of neointimal hyperplasia in vascular grafts by sustained perivascular delivery of paclitaxel

Neointimal hyperplasia associated with synthetic hemodialysis grafts

Contact Info

Product

Resources

About