Vein Graft Harvesting Induces Inflammation and Impairs Vessel Reactivity

Hinokiyama, Kazuhiro; Valen, Guro; Tokuno, Shinichi; Vedin, Jenny; Vaage, Jarle

doi:10.1016/j.athoracsur.2006.05.038

Cited by 42 publications

(28 citation statements)

References 21 publications

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“…Harvesting the vein graft is known to activate the graft endothelium [35]. Cell adhesion molecules have been shown to play a role in graft occlusion after coronary artery surgery, with their suppression shown to be protective [36].…”

Section: Being Blunted By Anti-inflammatory Mediators Such As Il-10mentioning

confidence: 99%

Endothelial Activation After Coronary Artery Bypass Surgery: Comparison Between On-Pump and Off-Pump Techniques

Vallely

Bannon

Bayfield

et al. 2010

Heart, Lung and Circulation

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Section: Being Blunted By Anti-inflammatory Mediators Such As Il-10mentioning

confidence: 99%

Endothelial Activation After Coronary Artery Bypass Surgery: Comparison Between On-Pump and Off-Pump Techniques

Vallely

Bannon

Bayfield

et al. 2010

Heart, Lung and Circulation

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“…As we studied vein surplus for bypass being directly harvested from the patient's leg, we therefore dealt with a vein injury model with altered endothelial functions which might directly impair the vein graft patency [34] .…”

Section: Discussionmentioning

confidence: 99%

Ex vivo Pulsatile Perfusion of Human Saphenous Veins Induces Intimal Hyperplasia and Increased Levels of the Plasminogen Activator Inhibitor 1

et al. 2010

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Vessel wall trauma induces vascular remodeling processes including the development of intimal hyperplasia (IH). To assess the development of IH in human veins, we have used an ex vivo vein support system (EVVSS) allowing the perfusion of freshly isolated segments of saphenous veins in the presence of a pulsatile flow which reproduced arterial conditions regarding shear stress, flow rate and pressure during a period of 7 and 14 days. Compared to the corresponding freshly harvested human veins, histomorphometric analysis showed a significant increase in the intimal thickness which was already maximal after 7 days of perfusion. Expression of the endothelial marker CD31 demonstrated the presence of endothelium up to 14 days of perfusion. In our EVVSS model, the activity as well as the mRNA and protein expression levels of plasminogen activator inhibitor 1, the inhibitor of urokinase-type plasminogen activator (uPA) and tissue-type plasminogen activator (tPA), were increased after 7 days of perfusion, whereas the expression levels of tPA and uPA were not altered. No major change was observed between 7 and 14 days of perfusion. These data show that our newly developed EVVSS is a valuable setting to study ex vivo remodeling of human veins submitted to a pulsatile flow.

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“…Various methods have been developed for the surgical harvest of saphenous veins for CABG with endoscopic harvest remains most commonly performed which leads to traction on the vein and injury to the endothelium and media [3][4][5]. After harvest, the veins are further Bprepared^prior to implantation by pressure distension [6], off-label marking with a surgical skin marker [7], and storing in a non-buffered solution [8], resulting in physiologic dysfunction, increased oxidative stress [9] and increased expression of genes that involved in inflammation and apoptosis [10][11][12]. Thus, minimizing operative injury to the conduit at the time of harvest and preparation improves conduit function [13] and may prevent vein graft failure.…”

Section: Introductionmentioning

confidence: 99%

P2X7R antagonism after subfailure overstretch injury of blood vessels reverses vasomotor dysfunction and prevents apoptosis

Luo

Feldman

McCallister

et al. 2017

Purinergic Signalling

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Human saphenous vein (HSV) is harvested and prepared prior to implantation as an arterial bypass graft. Injury and the response to injury from surgical harvest and preparation trigger cascades of molecular events and contribute to graft remodeling and intimal hyperplasia. Apoptosis is an early response after implantation that contributes the development of neointimal lesions. Here, we showed that surgical harvest and preparation of HSV leads to vasomotor dysfunction, increased apoptosis and downregulation of the phosphorylation of the anti-apoptotic protein, Niban. A model of subfailure overstretch injury in rat aorta (RA) was used to demonstrate impaired vasomotor function, increased extracellular ATP (eATP) release, and increased apoptosis following pathological vascular injury. The subfailure overstretch injury was associated with activation of p38 MAPK stress pathway and decreases in the phosphorylation of the anti-apoptotic protein Niban. Treatment of RA after overstretch injury with antagonists to purinergic P2X7 receptor (P2X7R) antagonists or P2X7R/pannexin (PanX1) complex, but not PanX1 alone, restored vasomotor function. Inhibitors to P2X7R and PanX1 reduced stretch-induced eATP release. P2X7R/PanX1 antagonism led to decrease in p38 MAPK phosphorylation, restoration of Niban phosphorylation and increases in the phosphorylation of the anti-apoptotic protein Akt in RA and reduced TNFα-stimulated caspase 3/7 activity in cultured rat vascular smooth muscle cells. In conclusion, inhibition of P2X7R after overstretch injury restored vasomotor function and inhibited apoptosis. Treatment with P2X7R/PanX1 complex inhibitors after harvest and preparation injury of blood vessels used for bypass conduits may prevent the subsequent response to injury that lead to apoptosis and represents a novel therapeutic approach to prevent graft failure.

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Vein Graft Harvesting Induces Inflammation and Impairs Vessel Reactivity

Cited by 42 publications

References 21 publications

Endothelial Activation After Coronary Artery Bypass Surgery: Comparison Between On-Pump and Off-Pump Techniques

Endothelial Activation After Coronary Artery Bypass Surgery: Comparison Between On-Pump and Off-Pump Techniques

Ex vivo Pulsatile Perfusion of Human Saphenous Veins Induces Intimal Hyperplasia and Increased Levels of the Plasminogen Activator Inhibitor 1

P2X7R antagonism after subfailure overstretch injury of blood vessels reverses vasomotor dysfunction and prevents apoptosis

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