Signs of patency in small vessel anastomosis

Acland, Richard

doi:10.1097/00006534-197309000-00046

Cited by 19 publications

(19 citation statements)

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“…Pulsation was observed when femoral circulation was restored and for up to 20 min (when the rats were sacrificed), indicating flow in the collagen tube. During this period, patency was further confirmed by performing the Acland milking test, 20 where we observed refilling of the distal femoral artery after emptying it of blood.…”

Section: Dried-and-crosslinked Tube Successfully Withstood Implantatimentioning

confidence: 72%

Generation, Endothelialization, and Microsurgical Suture Anastomosis of Strong 1-mm-Diameter Collagen Tubes

Nicolescu

et al. 2017

Tissue Engineering Part A

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Tissue-engineered vascular grafts that are based on reconstituted extracellular matrices have been plagued by weak mechanical strength that prevents handling or anastomosis to native vessels. In this study, we devise a method for making dense, suturable collagen tubular constructs of diameter £1 mm for potential microsurgical applications, by dehydrating tubes of native rat tail type I collagen and crosslinking them with 20 mM genipin. Crosslinked dense collagen tubes with 1 mm inner diameter yielded ultimate tensile strength of 342 -15 gF and burst pressure of 1313 -156 mm Hg, comparable to the strength of a rat femoral artery, and supported endothelial cell adhesion and growth. End-to-end anastomosis of 0.5-mm-diameter tubes to explanted arteries displayed anastomotic strength of 82 -21 gF, which is sufficient for surgical applications. In vivo implantation of cell-free tubes as interpositional grafts in the rat femoral circulation yielded stable anastomosis with blood flow for 20 min. Seeded dense collagen tubes represent a promising alternative to venous graft that can potentially be used to bridge between short artery stubs in replantation surgeries.

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Section: Dried-and-crosslinked Tube Successfully Withstood Implantatimentioning

confidence: 72%

Generation, Endothelialization, and Microsurgical Suture Anastomosis of Strong 1-mm-Diameter Collagen Tubes

Nicolescu

et al. 2017

Tissue Engineering Part A

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“…A single intravenous bolus of heparin (5 U in 100 L) was given immediately before reflow of the femoral artery. Patency of the grafted vessel was evaluated by mechanically emptying and observing refill downstream from the graft 25 immediately after repair and again at 1 and 5, 10, or 30 days after grafting.…”

Section: Vein Graft Modelmentioning

confidence: 99%

Murine Model of Neointimal Formation and Stenosis in Vein Grafts

Cooley

2004

ATVB

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Objective-Previous studies have suggested that neointimal formation, a central cause of vein graft stenosis, has several potential cell sources. It was hypothesized that neointimal cells arise primarily from the cells of the vein graft. Methods and Results-This study investigated vein graft neointimal cell origins using a model of vein-to-artery cross-transplantation between transgenic Rosa26 mice (constitutive expression of bacterial ␤-galactosidase marker gene) and wild-type mice. Vein-originating cells survived and make a major contribution to neointimal formation within the vein graft, mostly adjacent to the lumen/endothelium, suggesting an intimate association with endothelial cells. Key Words: bypass graft Ⅲ neointima Ⅲ Rosa26 Ⅲ thrombomodulin Ⅲ stenosis V ascular bypass surgery using vein grafts has become an established procedure for treating many conditions, most notably myocardial infarction (eg, coronary bypass) and limb claudication (eg, femoral-popliteal bypass grafting). 1,2 Despite high early success rates of these procedures, it is estimated that 20% to 50% of cases undergo stenotic occlusion of the graft within 5 years, 3-5 caused by an inward growth of neointimal cells. 6 Experimental models that mimic clinical vein grafting show a characteristic burst of neointimal cell proliferation early after grafting (3 to 7 days), which leads to a thickened intimal layer by 1 month. 7,8 This neointimal growth appears to stabilize beyond 1 to 2 months in animal models 9,10 and does not create significant graft stenosis at any time, thus differing from the clinical progression of this complication. See page 1147The source of neointimal cells remains controversial. Studies using arterial injury models (eg, balloon angioplasty) have presented evidence for medial smooth muscle cells, adventitial (myo)fibroblasts, and blood-borne stem cells as major contributors to the neointima. 11-15 Studies using vein graft models have supported adjacent arterial media as a major source for neointimal cells. 7,16 Arterial and organ allotransplantation models have found that circulating progenitor cells and adjacent (recipient) arterial media are the major contributors to transplant-associated neointimal formation. 15,[17][18][19] A recent study using a murine vein graft model demonstrated that the neointimal cells within the graft arise from both the vein graft and the recipient artery. 20 The following study confirms this result using a new murine model that has direct analogy to clinical vein grafting and stenosis. Furthermore, the findings show that neointima cells from the vein graft arise from and proliferate predominantly at the innermost (luminal) aspect, suggesting involvement of vein-derived endothelial cells. Methods Vein Graft ModelA new model of vein graft transplantation in mice was developed by the author and is similar to recently described murine vein graft models 20 -22 but uses a smaller-diameter graft, a branch of the jugular vein, interpositioned to the femoral artery. This model has more clinical analogy...

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“…Free vascularized transplants have been used for more than 30 years in many fields of surgery for reconstruction and repair (Acland, 1972(Acland, , 1977Daniel and Taylor, 1973;Acland and Trachtenberg, 1977;Biemer and Duspiva, 1980). These transplants can be threatened by complications at the anastomoses, for instance by thrombosis in the early postoperative phase.…”

Section: Introductionmentioning

confidence: 99%