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BIOSPUN VASCULAR GRAFTS: IN VIVO EVALUATION OF A NOVEL SMALL‐DIAMETER BIOACTIVE NANOFIBROUS VASCULAR GRAFT FOR ARTERIAL RECONSTRUCTION
Author(s) -
Contreras Mauricio Antonio,
Phaneuf Mathew Douglas,
Wu Shengqian,
Bide Martin J.,
LoGerfo Frank W.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.605
Subject(s) - thrombogenicity , thrombus , intimal hyperplasia , medicine , anastomosis , vascular graft , lumen (anatomy) , in vivo , blood vessel , antithrombotic , transplantation , surgery , thrombosis , biomedical engineering , cardiology , biology , microbiology and biotechnology , smooth muscle
Prosthetic vascular grafts fail due to thrombus formation and anastomotic intimal hyperplasia. Objective: Our goal was to assess graft patency and healing of a small‐diameter, bioactive nanofibrous vascular graft (BioSpun™). Methods: BioSpun grafts, synthesized via a proprietary technology, contained both antithrombotic and endothelial‐cell specific mitogenic properties. BioSpun™ grafts were interposition in the common carotid arteries of canines (n=12), with a woven polyester graft serving as the contralateral control. Grafts were retrieved at 7, 14 and 30 days (n=3), fixed in formalin and processed for histology. Results: Patency of both grafts was comparable (100%) at all time intervals. Histological evaluation of the BioSpun™ grafts revealed an increased number of blood vessels throughout the graft wall and increased cellular penetration across the graft lumen, with minimal thrombus formation. In contrast, control grafts failed to exhibit these healing characteristics. Conclusions: These results demonstrate the feasibility to design a prosthetic vascular graft capable of interacting with the recipient arterial vessel. Thus, this novel small‐diameter prosthetic graft could have a significant impact on small vessel repair and replacement due to its reduced thrombogenicity and promotion of cellular incorporation with subsequent healing. Support: NIH SBIR 2 R44 HL074771‐02