Influence of Perioperative Storage Solutions on Long-Term Vein Graft Function and Morphology

Hagen, Per Otto

doi:10.1007/bf02018863

Cited by 25 publications

(12 citation statements)

References 29 publications

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“…In contrast, rabbit vein grafts have been reported to show progressively decreased sensitivity with time after implantation, and a similar decreased sensitivity has also been reported in long-term canine vein grafts. However, in a recent study we reported a supersensitivity of the rabbit arterial vein graft at 2 and 4 weeks after implantation, contrary to previous results [18]. The responses to norepinephrine in both arterial vein grafts and venovenous grafts (grafts placed into the venous circulation) show an equivalent increase in sensitivity when compared with native jugular veins [19].…”

Section: Figmentioning

confidence: 63%

Functional Characterization of α1-Adrenergic Receptors in Experimental Vein Grafts

Huynh¹,

Hagen²

1999

Journal of Surgical Research

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Section: Figmentioning

confidence: 63%

Functional Characterization of α1-Adrenergic Receptors in Experimental Vein Grafts

Huynh¹,

Hagen²

1999

Journal of Surgical Research

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“…Injury to the graft, beginning at the time of harvest, may initiate endothelial dysfunction that in turn promotes platelet adherence, activation, and thrombosis. 33 Once implanted, the vein is subject to higher blood flow; greater longitudinal shear stress; and increased circumferential, radial, and pulsatile deformation and stress. 17 These factors may impair venous endothelial function further and result in decreases in both nitric oxide and prostacyclin activity.…”

Section: Discussionmentioning

confidence: 99%

Plasminogen Is Not Required for Neointima Formation in a Mouse Model of Vein Graft Stenosis

Shi

Patel

Zhang

et al. 1999

Circulation Research

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Abstract-Recent studies of mice that lack plasminogen have identified a critical role for this zymogen in arterial remodeling.To permit the use of these (and other) genetically modified mice in the analysis of venous injury, we developed a model in which a patch cut from the external jugular vein of a mouse is grafted to repair a surgically created defect in its carotid artery. In wild-type mice, the venous graft showed initial endothelial denudation and formation of a neointima that progressively and reproducibly expanded in a manner analogous to human vein graft disease, albeit at an accelerated pace. This neointima occupied 37Ϯ4.6% of the vessel lumen at day 7 and 66Ϯ5.7% at day 20. The proliferative index of neointimal cells assessed by proliferating cell nuclear antigen staining was 50.6Ϯ3.6% at day 7 and 15.2Ϯ2.0% at day 20. CD45-positive leukocytes and ␣-actin-positive smooth muscle cells accounted for 9.5Ϯ1.0% and 9.9Ϯ1.1% of intimal area at day 7, respectively, with the latter increasing to 40.9Ϯ2.6% at day 20. Collagen accounted for 6.8Ϯ0.7% of intimal area at day 7 and 20.7Ϯ1.8% at day 20. Surprisingly, even though arterial neointima formation due to electrostatic and immune-mediated injury is impaired in plasminogen -/-mice, in our study vein graft neointima formation in these mice was not significantly different from that in controls (70.9Ϯ6.4 versus 65.6Ϯ4.4% luminal occlusion, PϭNS). Thus, plasmin proteolysis, although critical in extracellular matrix degradation and cellular migration after arterial injury, does not appear to be so important in vein graft neointima formation, perhaps because of the relative lack of structural barriers to cellular migration in the normal vein wall. This novel model of vein graft injury should be useful for further studies of differences in the response to injury of arterial and venous tissues. (Circ Res. 1999;84:883-890.)

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“…Importantly, these novel insights into vein graft biology derive from a murine vein graft system that we have shown to model human vein grafts, with regard to their surgical anastomoses as well as the distribution, composition and extent of neointimal hyperplasia within the grafts. 12 Sources of graft-extrinsic neointimal cells in our murine model remain to be determined, but potential sources include migrating vascular cells from the adjacent carotid artery, 20 as well as progenitor cells infiltrating the graft through either circulating blood (vasa vasora 21 or transendothelial diapedesis 22 ) or postsurgical adventitial adhesions. Surgical trauma at the anastomoses activates SMCs of the adjacent artery to proliferate and ultimately migrate into vein grafts-a process clearly delineated in rat iliac vein grafts.…”

Section: Discussionmentioning

confidence: 99%

Graft-Extrinsic Cells Predominate in Vein Graft Arterialization

Zhang

Freedman

Brian

et al. 2004

ATVB

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Objective-Vein graft disease involves neointimal smooth muscle cells, the origins of which are unclear. This study sought to characterize and quantitate vein graft infiltration by cells extrinsic to the graft in a mouse model of vein graft disease. Methods and Results-Inferior vena cava-to-carotid artery interposition grafting between C57Bl/6 and congenic ␤-galactosidase-expressing ROSA26 mice was performed. Vein grafts were harvested 6 weeks postoperatively and stained with X-gal. More than 60% of neointimal cells derived from the recipient, and 50% of these cells expressed smooth muscle ␣-actin.

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Influence of Perioperative Storage Solutions on Long-Term Vein Graft Function and Morphology

Cited by 25 publications

References 29 publications

Functional Characterization of α1-Adrenergic Receptors in Experimental Vein Grafts

Functional Characterization of α1-Adrenergic Receptors in Experimental Vein Grafts

Plasminogen Is Not Required for Neointima Formation in a Mouse Model of Vein Graft Stenosis

Graft-Extrinsic Cells Predominate in Vein Graft Arterialization

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