Patency and structural changes in cryopreserved arterial grafts used as vessel substitutes in the rat

Pascual, Gemma; Martinez, Sylvia; Rodrı́guez, Marta; Serrano, Natalia; Buján, Julia

doi:10.1016/j.jss.2004.10.016

Cited by 15 publications

(15 citation statements)

References 19 publications

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“…[38] Despite numerous efforts that have been made to improve the vascular allograft cryopreservation, poor results were observed especially due to changes in the mechanical properties of the tissue. [7,8,12] Moreover, similar mechanical properties of the graft and the recipient vascular conduit appeared to be important to prevent intimae hyperplasia, which corresponds to an increase of the cell number and of the size of the tissue, occlusion, and dilatation of the blood vessels. [39,40] In fact, the cryopreservation procedure as well as the enzymatic treatment may also alter the collagen/elastin network and modify the mechanical properties of the arteries.…”

Section: Full Papermentioning

confidence: 99%

Re‐endothelialization of Human Umbilical Arteries Treated with Polyelectrolyte Multilayers: A Tool for Damaged Vessel Replacement

Kerdjoudj

Boura

Moby

et al. 2007

Adv Funct Materials

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The use of cryopreserved arteries for vascular tissue engineering provides a promising way for vessel replacement. Unfortunately cryopreservation induces structural changes that strongly modify the mechanical properties and alter the thrombogenicity of the vessel after implantation. We present here a new procedure to treat the inner coating of cryopreserved arteries with poly(sodium‐4‐styrene sulfonate)/poly(allylamine hydrochloride) polyelectrolyte multilayers. We show that this treatment improves the mechanical properties of the cryopreserved vessel. It also allows the adhesion and spreading of endothelial cells so that the internal structure of the vessel closely resembles that of fresh arteries. Finally, we verify by PECAM‐1 and von‐Willebrand‐factor (vWF) expression that this treatment preserves the phenotype of the endothelial cells. This study should open new routes towards the development of future, new biocompatible tissue substitutes allowing long‐term functionality after implantation.

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Section: Full Papermentioning

confidence: 99%

Re‐endothelialization of Human Umbilical Arteries Treated with Polyelectrolyte Multilayers: A Tool for Damaged Vessel Replacement

Kerdjoudj

Boura

Moby

et al. 2007

Adv Funct Materials

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“…This neointima increased in thickness until 90/180 days after implantation, when cell loss and the consequent degradation of the medial layer took place. This last process cannot be ascribed to the immune response since it has been reported to similarly occur in a syngeneic transplant model [11]. It is likely that the grafting process induces cell or perhaps molecular changes in the extracellular matrix that impair the onset of the proliferative and migratory response.…”

Section: Discussionmentioning

confidence: 99%

Role of Lysyl Oxidases in Neointima Development in Vascular Allografts

Rodríguez

Pascual²,

Cifuentes³

et al. 2010

J Vasc Res

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Background: Extracellular matrix deposition is the main factor inducing stenotic lesions in arterial grafts. Lysyl oxidases (LOX) play a key role in stabilizing collagen and elastin. Objective: To examine the repair response to arterial allografts in terms of LOX expression and collagen/elastin deposition using LOX inhibitors. Methods: Lewis/Fisher-344 rats were used as donors/recipients. Donor segments were grafted to the right iliac artery of recipients and retrieved 14/30 (short-term) or 90/180 days (long-term) after surgery. One group of animals was injected with a potent irreversible LOX inhibitor daily for 30 days. Results: Intimal hyperplasia increased in thickness until 90/180 days postsurgery. Elastin showed great expression in the neointima at 14/30 days and in the media at 90/180 days. LOX/LOXL1 were similarly expressed in the arterial wall during the first month. In the long term, their overexpression was confined to neointimal layers. At 14 days, collagen types I/III were identified in the grafts. The neointima acquired collagen I over time. In the group of animal treated with the LOX inhibitor, intimal hyperplasia was significantly inhibited. Conclusion: LOX were overexpressed in late stages of intimal hyperplasia in the allografts. LOX inhibitors prevented the development of the neointimal layer, such that their modulation could reduce the excessive extracellular matrix deposition that leads to stenosis.

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“…Cryopreserved arteries are used for this purpose [7,8]. Cryogenic temperatures maintain vascular integrity over prolonged periods of time.…”

Section: Introductionmentioning

confidence: 99%

“…The susceptibility to cracking is aggravated when vessels are stored at very low temperatures and then quickly thawed [15,16]. Leaks at the anastomotic sites are more common than in the non-cryopreserved arteries [8].…”

Section: Introductionmentioning

confidence: 99%