Perivenous support reduces early changes in human vein grafts: Studies in whole blood perfused human vein segments

Stooker, Wim; Niessen, Hans W.M.; Baidoshvili, Alexi; Wildevuur, W.R.; Hinsbergh, Victor W.M. van; Fritz, J K; Wildevuur, Charles; Eijsman, L.

doi:10.1067/mtc.2001.111656

Cited by 45 publications

(39 citation statements)

References 27 publications

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“…SMCs represent the most prominent cellular element of the intimal lesion (19), and immunohistochemical analysis by our group (Fig. 6A) and others (20,21) indicates that SMCs, rather than endothelium, can make contact with flowing blood in human vein grafts. It is possible therefore that the SMC response to flow may influence shear-dependent thickening in the de-endothelialized vein graft.…”

Section: Induction Of C-jun In Smcs Exposed To Fluid Shear Stress Is mentioning

confidence: 99%

c-Jun Regulates Shear- and Injury-inducible Egr-1 Expression, Vein Graft Stenosis after Autologous End-to-Side Transplantation in Rabbits, and Intimal Hyperplasia in Human Saphenous Veins

Waldman

Khachigian

2010

Journal of Biological Chemistry

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Coronary artery bypass graft failure represents an unsolved problem in interventional cardiology and heart surgery. Late occlusion of autologous saphenous vein bypass grafts is a consequence of neointima formation underpinned by smooth muscle cell (SMC) migration and proliferation. Poor long term patency and the lack of pharmacologic agents that prevent graft failure necessitate effective alternative therapies.

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Section: Induction Of C-jun In Smcs Exposed To Fluid Shear Stress Is mentioning

confidence: 99%

c-Jun Regulates Shear- and Injury-inducible Egr-1 Expression, Vein Graft Stenosis after Autologous End-to-Side Transplantation in Rabbits, and Intimal Hyperplasia in Human Saphenous Veins

Waldman

Khachigian

2010

Journal of Biological Chemistry

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“…Stooker et al (59) placed seven pairs of human saphenous veins harvested using the no-touch technique in a perfusion circuit and perfused them with oxygenated human blood for 60 min at 60 mmHg of nonpulsatile pressure. One-half of the veins were placed inside an external stent before being placed in the circuit.…”

Section: External Stentmentioning

confidence: 99%

Coronary vein graft disease: Pathogenesis and prevention

Parang

Arora

2009

Canadian Journal of Cardiology

155

109

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“…18 Briefly, vein segments (n ϭ 6 for each time point; 1 and 6 hours) were placed in a loop of the extracorporeal circulation during bypass surgery and were exposed to autologous blood under flow (nonpulsatile), and the intraluminal pressure was allowed to approximate the arterial pressure of the patient. To study the effect of overdistension on bypass veins, vein segments were perfused in the presence or absence of an external stent (polytetrafluoroethylene graft).…”

Section: Human Tissue Specimensmentioning

confidence: 99%

TR3 Nuclear Orphan Receptor Prevents Cyclic Stretch-Induced Proliferation of Venous Smooth Muscle Cells

Waard

Arkenbout

Vos

et al. 2006

The American Journal of Pathology

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In coronary artery bypass surgery , the patency of arterial grafts is higher than that of venous grafts because of vein-graft disease , which involves excessive proliferation of venous smooth muscle cells (SMCs) and subsequent accelerated atherosclerosis. We studied the function of TR3 nuclear orphan receptor (TR3) in the early response of SMCs to mechanical strain , a major initiator of vein-graft disease. We demonstrate that TR3 expression is induced in human saphenous vein segments exposed ex vivo to whole-blood perfusion under arterial pressure. Cultured venous SMCs challenged by cyclic stretch displayed TR3 induction and enhanced DNA synthesis , whereas SMCs derived from the internal mammary artery remained quiescent. Small-interfering RNA-mediated knockdown of TR3 and adenovirus-mediated overexpression of TR3 in venous SMCs enhanced and abolished stretch-induced DNA synthesis , respectively. Accordingly, in organ cultures of wild-type murine vessel segments exposed to cyclic stretch, p27Kip1 was down-regulated, whereas expression of this cell cycle inhibitor was unaffected by cyclic stretch in TR3-transgenic vessels, concordant with a lower proliferative response. Finally, stretch-mediated proliferation was inhibited by 6-mercaptopurine, an agonist of TR3. In conclusion, TR3 represents inhibitory mechanisms to restrict venous SMC proliferation and may contribute to prevention of veingraft disease.

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Perivenous support reduces early changes in human vein grafts: Studies in whole blood perfused human vein segments

Abstract: In our in vitro closed-loop model, reproducible vessel wall changes were observed in all human vein graft specimens studied. The beneficial effect of perivenous support could also be established for the human greater saphenous vein, providing a basis for clinical application.

Cited by 45 publications

References 27 publications

c-Jun Regulates Shear- and Injury-inducible Egr-1 Expression, Vein Graft Stenosis after Autologous End-to-Side Transplantation in Rabbits, and Intimal Hyperplasia in Human Saphenous Veins

c-Jun Regulates Shear- and Injury-inducible Egr-1 Expression, Vein Graft Stenosis after Autologous End-to-Side Transplantation in Rabbits, and Intimal Hyperplasia in Human Saphenous Veins

Coronary vein graft disease: Pathogenesis and prevention

TR3 Nuclear Orphan Receptor Prevents Cyclic Stretch-Induced Proliferation of Venous Smooth Muscle Cells

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