Preserved endothelial integrity and nitric oxide synthase in saphenous vein grafts harvested by a ‘no-touch’ technique

Tsui, Janice; Souza, Domingos; Filbey, Derek; Bomfim, Vollmer; Dashwood, Michael R.

doi:10.1046/j.0007-1323.2001.01855.x

Cited by 92 publications

(72 citation statements)

References 17 publications

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“…Stretching of veins during harvesting and preparation for grafting can lead to partial loss of ECs, 34 whereas a "no touch" technique for vein harvest leads to the preservation of ECs. 35,36 Veins grafted into the arterial circulation are also exposed to a sudden increase in blood flow, which elevates shear stress at the vascular wall. Venous ECs are activated rapidly by the application of arterial shear stress, [37][38][39][40][41] and it is likely that this process contributes to early inflammatory processes in vein grafts.…”

Section: Discussionmentioning

confidence: 99%

Dexamethasone Arterializes Venous Endothelial Cells by Inducing Mitogen-Activated Protein Kinase Phosphatase-1

et al. 2011

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Background-Vein grafting in coronary artery surgery is complicated by a high restenosis rate resulting from the development of vascular inflammation, intimal hyperplasia, and accelerated atherosclerosis. In contrast, arterial grafts are relatively resistant to these processes. Vascular inflammation is regulated by signaling intermediaries, including p38 mitogen-activated protein (MAP) kinase, that trigger endothelial cell (EC) expression of chemokines (eg, interleukin-8, monocyte chemotactic protein-1) and other proinflammatory molecules. Here, we have tested the hypothesis that p38 MAP kinase activation in response to arterial shear stress (flow) may occur more readily in venous ECs, leading to greater proinflammatory activation. Methods and Results-Comparative reverse-transcriptase polymerase chain reaction and Western blotting revealed that arterial shear stress induced p38-dependent expression of monocyte chemotactic protein-1 and interleukin-8 in porcine jugular vein ECs. In contrast, porcine aortic ECs were protected from shear stress-induced expression of p38-dependent chemokines as a result of rapid induction of MAP kinase phosphatase-1. However, we observed with both cultured porcine jugular vein ECs and perfused veins that venous ECs can be protected by brief treatment with dexamethasone, which induced MAP kinase phosphatase-1 to suppress proinflammatory activation. 1 This process is coordinated by the simultaneous activation of c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein (MAP) kinases 2 and nuclear factor-B (NF-B) 3 signaling pathways, which cooperate to induce and stabilize proinflammatory transcripts in vascular ECs. 4,5 Clinical Perspective on p 532 Conclusions-ArterialThe susceptibility of blood vessels to inflammatory processes varies according to their anatomic location. This has been attributed to local differences in hemodynamics 6,7 ; differences in the structure and physiology of blood vessels also play an important role. 8,9 This is exemplified in bypass grafting in which arteries and veins respond differently to arterial flow. Although vein grafts are commonly used as conduits in cardiac and vascular surgery, 10 their use is commonly complicated by intimal hyperplasia and accelerated atherosclerosis, which cause late failure rates of up to Received October 14, 2009; accepted November 15, 2010. From the British Heart Foundation Cardiovascular Sciences Unit, National Heart and Lung Institute (M.Z., L.A.L., H.C., O.R., J.C.M., D.O.H., P.C.E.), Department of Cardiothoracic Surgery (P.P.P., J.R.A., J.W.M., A.T.C.), Department of Bioengineering (R.K., N.F.), and Department of Biosurgery and Surgical Technology (T.A.) To gain insight into intrinsic molecular mechanisms underlying the differential responses of arteries and veins to grafting, we compared the effects of arterial shear stress on proinflammatory activation of venous and arterial ECs. We found that arterial but not venous ECs were protected from proinflammatory activation in response to the rapid induction of high...

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Section: Discussionmentioning

confidence: 99%

Dexamethasone Arterializes Venous Endothelial Cells by Inducing Mitogen-Activated Protein Kinase Phosphatase-1

et al. 2011

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“…The endothelial injury may occur owing to mechanical reason such as excesses separation, stretch and distension, as well as chemical reason such as hypoxia during preservation, ischemia-reperfusion and condition of storage solution. In previous study, prevention of mechanical injury was emphasized in protection of vein graft, including applying "no touch" and endoscopic mimimally invasive techniques, addition of vasodilator to avoid vascular spasmodism, as well as retaining extravascular tissue [3] . Thatte et al [4] have reported that endothelial cell activity of HSV was affected in several minutes of preservation and after 1 h of preservation endothelial cells phenotype changed leading to attenuating of anticoagulation, increasing of permeability and adhesion, thus endothelial cells appeared proinflammatory characteristics.…”

Section: Discussionmentioning

confidence: 99%

“…Nitric oxide (NO) is produced from L-arginine by nitric oxide synthase (NOS), which regulate vascular tension, sustain normal vascular physiologic function, decrease expression of adhesion molecules as well as inhibit leucocyte-endothlium interaction and platelet aggregation. Tsui et al reported that harvesting HSV by using minimally invasive techniques may preserve endothelial NOS (eNOS) expression and NO production as well [3] . In this study we found that after preservating 1 h in solution with Troglitazone, eNOS expression of HSV is significantly higher than control group, meanwhile vascular cell adhesion molecule-1(VCAM-1) and intercellular adhesion molecule-1(ICAM-1) expression of HSV is significantly lower than control group leading to conclusion that preservation solution with Troglitazone may offer better protective function to HSV.…”

Section: Discussionmentioning

confidence: 99%

Effect of Troglitazone on expression of adhesion molecules and eNOS in human saphenous vein gaft

Chen

Zhang

et al. 2007

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

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To investigate whether peroxisome proliferators-activated receptor-gamma (PPARgamma) ligand Troglitazone can reduce endothelial injury and activation during storage of harvested saphenous vein grafts. Segments of human saphenous vein graft were collected from 9 patients undergoing coronary bypass surgery and then divided into two equal parts of control and test specimens, were stored in either heparinized blood (control group) or heparinized blood containing 20 mumol/L troglitazone (test group) for 1 h at room temperature. Tissue distribution and protein expression of VCAM-1, ICAM-1, and endothelial nitric oxide synthase (eNOS) were compared using immunohistochemistry and Western blot analysis. Myeloperoxidase (MPO) activity, a marker of neutrophil sequestration in human saphenous vein grafts, was also measured in each group. The expression of ICAM-1 (753+/-132 versus 7201+/-934; P<0.01), VCAM-1 (3731+/-294 versus 8292+/-793; P<0.01), and MPO activity (1.52+/-0.42 U/g, 5.04+/-1.26 U/g P<0.01) were significantly lower in test group. In contract, eNOS expression (7983+/-834 versus 3989+/-1008; P<0.01) was significantly higher in test group. PPARgamma ligand troglitazone might reduce endothelial injury during the storage period of human saphenous vein grafts.

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“…The goal is to preserve endothelial and smooth muscle cell presence and function in the graft, with a presumed outcome of reduced maladaptive neointimal overgrowth, though early prevention of thrombosis is also a rationale. Endothelial preservation will maintain nitric oxide and prostacyclin generation, 21 critical factors for sustaining function, patency, and vascular integrity. The effect of no-touch graft harvesting on subsequent bypass surgery outcome is difficult to evaluate, given that it represents differences in personal surgical technique and that endothelial cells cannot be directly seen or tracked following clinical graft placement.…”

Section: Graft Ec Integritymentioning

confidence: 99%

“…Many vascular surgeons advocate a "no touch" technique [19][20][21] for vein graft harvest, in an effort to minimize vein graft iatrogenic injury. The goal is to preserve endothelial and smooth muscle cell presence and function in the graft, with a presumed outcome of reduced maladaptive neointimal overgrowth, though early prevention of thrombosis is also a rationale.…”

Section: Graft Ec Integritymentioning

confidence: 99%

Experimental Vein Graft Research: A Critical Appraisal of Models

Cooley¹

2015

Heart Res Open J

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Experimental models of vein grafting need to have specific relevance to the clinical complications encountered in coronary artery bypass grafting: acute thrombosis, neointimaassociated stenosis, and progression of late-forming atherosclerotic lesions. Despite extensive use, many of these experimental models lack endpoint measures with clear analogies to their clinical counterparts and may in fact target the wrong (patho) physiologic process. Model selection is critical to further progress toward preventing these all too prevalent complications used for heart revascularization.

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Preserved endothelial integrity and nitric oxide synthase in saphenous vein grafts harvested by a ‘no-touch’ technique

Abstract: Some of the sites with potential for nitric oxide release in vivo are removed during conventional saphenous vein harvesting. These sites were preserved after no-touch harvesting, suggesting the potential to improve coronary artery bypass graft patency.

Cited by 92 publications

References 17 publications

Dexamethasone Arterializes Venous Endothelial Cells by Inducing Mitogen-Activated Protein Kinase Phosphatase-1

Dexamethasone Arterializes Venous Endothelial Cells by Inducing Mitogen-Activated Protein Kinase Phosphatase-1

Effect of Troglitazone on expression of adhesion molecules and eNOS in human saphenous vein gaft

Experimental Vein Graft Research: A Critical Appraisal of Models

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