Nature and pressure dependence of damage induced by distension of human saphenous vein coronary artery bypass grafts

Angelini, Gianni D; Passani, Stefano L; Breckenridge, I. M.; Newby, Andrew C.

doi:10.1093/cvr/21.12.902

Cited by 92 publications

(48 citation statements)

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“…Preparation of the veins before implantation is associated with a limited loss of endothelial cells, in contrast with the findings of Angelini et al (1987Angelini et al ( , 1989, who reported a much higher endothelial cell loss. However, they estimated the endothelial cell loss after a pharmacological experiment and used a different preparation technique.…”

Section: Discussioncontrasting

confidence: 64%

The modulation of smooth muscle cell phenotype is an early event in human aorto-coronary saphenous vein grafts

Kockx

Cambier

Bortier³

et al. 1992

Vichows Archiv A Pathol Anat

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The morphological changes in human vein grafts occurring in the first days after a coronary bypass operation (CBP) are rarely reported in the literature. Sections of aorto-coronary vein grafts from 11 patients who died during the first 10 days after a CBP were obtained at autopsy. The number of vein grafts per patient ranged from 1 to 4, yielding a total of 28 vein grafts. The early changes in the vein grafts have been studied by light microscopy, immunohistochemistry, transmission and scanning electron microscopy. The study demonstrates that soon after grafting, the vein wall is infiltrated by polymorphonuclear leucocytes (PMN). At 24 h the endothelium shows extensive desquamation. The massive migration of PMN through the venous wall occurs simultaneously with the endothelial damage. The circular layer of the media is severely damaged, resulting in a loss of smooth muscle cells (SMC). The remaining SMC in this layer show a change toward the synthetic phenotype and a reduced expression of alpha-smooth muscle actin. These early changes in the SMC function may initiate the process of fibrosis in the intima and the media of the vein grafts.

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Section: Discussioncontrasting

confidence: 64%

The modulation of smooth muscle cell phenotype is an early event in human aorto-coronary saphenous vein grafts

Kockx

Cambier

Bortier³

et al. 1992

Vichows Archiv A Pathol Anat

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“…22 This type of distension has been shown to cause morphological and biochemical alterations in the vessel wall. 23,24 In addition, several hemodynamic changes occur in the SV after implantation into the coronary circulation, including alterations in blood flow, transmural pressure, shear stress, and radial stress. 25 In addition, interruption of the vasa vasorum during explantation of vein is likely to cause ischemic necrosis.…”

Section: Discussionmentioning

confidence: 99%

Mechanical Stretch Induces Phosphorylation of p38-MAPK and Apoptosis in Human Saphenous Vein

Cornelissen

Armstrong

Holt

2004

ATVB

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Objective-Failure of saphenous vein grafts remains a major limitation of coronary bypass surgery. The aims of the present study were to determine whether pressure distension of human saphenous vein induces the activation of p38-MAPK and to determine its role in apoptosis. Methods and Results-Phosphorylated p38 was detected at basal levels in human saphenous vein obtained immediately after harvesting. Distended saphenous vein showed significantly higher levels of phosphorylated p38 compared with control vein (PϽ0.01) and nondistended saphenous vein maintained for 3 and 6 hours after harvesting (both PϽ0.01 A utologous saphenous vein (SV) is the commonest conduit used for peripheral and coronary artery bypass grafting. However, 30% to 50% of vein grafts become occluded by 10 years. 1 The causes of vein graft occlusion are thrombosis in the early stages, and later the proliferation and migration of intimal smooth muscle cells along with the deposition of extracellular matrix leading to myointimal hyperplasia. 1 The precise cellular mechanisms involved in these processes remain unclear; however, surgical trauma to the vessel, including the stretch that occurs during manual distension before implantation, as well as implantation of the vein into the arterial circulation may be important.Apoptosis is reported to occur in pathological SV grafts, where it is thought to be involved in the transformation of a smooth muscle cell-rich myointimal thickening toward a fibrous cell-poor intimal thickening. 2,3 Apoptosis has also been shown to occur in tissue remodeling, associated with longitudinal stretch (axial strain) in rabbit carotid arteries. 4 We have previously shown that apoptosis is induced in pressure-distended human SV and is associated with increased vessel wall expression of the transcription factor c-fos, a downstream component of various signaling cascades. 5 In cultured porcine vascular smooth muscle cells (VSMCs), cyclic stretch has been shown to cause an increase in apoptosis, accompanied by a sustained activation of the mitogen-activated protein kinases (MAPK) JNK and p38. 6 In vitro studies using cultured smooth muscle cells have shown that mechanical stretch can activate ras/rac/p38 signal pathways 7 and p38 phosphorylates p53, which is responsible for mechanical stress-induced apoptosis. 8 In addition, the application of biomechanical stress has been shown to increase apoptosis in mouse vein grafts, and this occurs via p38 activation. 9 MAPKs are proline-directed serine/threonine kinases activated by dual phosphorylation on threonine and tyrosine residues in response to a wide variety of extracellular stimuli. The JNK and p38 MAPK signaling cascades are activated in response to cellular stress and certain cytokines via the activation of G protein coupled receptors 10 and are known to be involved in apoptosis. 11 Overexpression of MAPKs upstream of p38, such as MKK-3, leads to sustained activation of p38 and apoptosis. 12,13 However, ERK-MAPK is downregulated during apoptosis and upregulated during cellula...

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“…It has been shown that the level of intimal hyperplasia is directly linked to the degree of endothelial denudation, which, in vein grafts is caused by luminal distension during surgery, ischemia, damage at surgical anastomoses and continued physical trauma under arterial conditions (2)(3)(4). Moreover arterial tangential pressure, medial damage and thickening as well as shear stress changes and altered fl ow patterns are involved in the development of intimal hyperplasia (5)(6)(7).…”

mentioning

confidence: 99%

Tacrolimus inhibits intimal hyperplasia in arterialised veins in rats

Varga¹,

Matia²,

Lodererová³

et al. 2012

BLL

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Abstract:Objectves: We investigated whether tacrolimus (FK506) can inhibit neointimal formation in arterialised vein grafts in rats. Methods: Lewis iliolumbar veins were implanted into the abdominal aorta of isogeneic rats. Animals in the treatment groups had daily intramuscular injections of tacrolimus at 0.2 mg/kg (group B) and 0.1 mg/kg (Group C), respectively. The control group A had no treatment. Light microscope evaluations of arterialised vein grafts were performed 30 days after operation. We determined the presence of endothelial cells, the thickness of intima and media, and the degree of infi ltration by MHC class II positive, CD4 positive, and CD8 positive cells into the adventitia. Results: The intimal thickness in group B (5.0±1.0 μm) was statistically lower (P < 0.05) when compared to group C (7.0±3.0 μm). The intimal thickness in untreated group A (12.7±7.0 μm) was statistically higher (P < 0.01) when compared to both treated groups B and C, respectively. The medial thickness and degree of adventitial infi ltration by MHC class II positive, CD8 positive, and CD4 positive cells did not differ between groups. Conclusion: Treatment with tacrolimus (FK506) showed a dose dependant inhibition of neointimal hyperplasia in arterialised vein grafts in rats (Tab. 1, Fig. 3, Ref. 22). Full Text in free PDF www.bmj.sk.

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Nature and pressure dependence of damage induced by distension of human saphenous vein coronary artery bypass grafts

Cited by 92 publications

References 0 publications

The modulation of smooth muscle cell phenotype is an early event in human aorto-coronary saphenous vein grafts

The modulation of smooth muscle cell phenotype is an early event in human aorto-coronary saphenous vein grafts

Mechanical Stretch Induces Phosphorylation of p38-MAPK and Apoptosis in Human Saphenous Vein

Tacrolimus inhibits intimal hyperplasia in arterialised veins in rats

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