Endothelial activation in patients with chronic venous disease

Saharay, M.; Shields, D. A.; Georgiannos, Stavros N; Porter, John B.; Scurr, J. H.; Smith, Phillip D.

doi:10.1016/s1078-5884(98)80039-7

Cited by 83 publications

(70 citation statements)

References 27 publications

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“…They have already been used as markers of venous hypertension. 6 ACE was also significantly influenced in situ in the varicose vein and at distance in the brachial vein in response to blood stasis in the varicose vein. Therefore, as with sVCAM-1, ACE activity could be a systemic marker of blood stasis-induced endothelial protein shedding in the varicose vein.…”

Section: Discussionmentioning

confidence: 98%

“…Similarly, previous clinical investigations demonstrated the involvement of leukocyte activation in chronic venous ulcers. 5,6 Therefore, in view of this hypothesis, the objective of the present clinical investigation was to further evaluate intermediate biological markers of these interactions induced by blood stasis in varicose veins. For this purpose, oxygen partial pressure (PVO 2 ) and 12 biological markers were measured in blood sampled from varicose veins and paired brachial veins (as control), before and after induction of postural blood stasis.…”

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confidence: 99%

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Plasma Matrix Metalloproteinase-9 as a Marker of Blood Stasis in Varicose Veins

et al. 2002

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Background-Possible intermediate circulating markers linking blood stasis to vein remodeling were explored in patients with varicose veins in the lower limbs. Methods and Results-Blood was sampled at rest (supine position) and after a stasis of 30 minutes both in the varicose vein (limbs hanging down) and in the brachial vein (arm hanging down) as a paired control. Several endothelial and leukocyte markers were measured in plasma with the use of ELISA kits. Angiotensin-converting enzyme activity was determined by use of a specific substrate. Matrix metalloproteinases (MMPs) 9 and 2 were evaluated with the use of gelatin zymography. No markers were significantly modified after 30 minutes of blood stasis in the brachial vein. After 30 minutes of blood stasis in the varicose vein, oxygen partial pressure decreased (PϽ0.01). Although thrombomodulin, von Willebrand factor, vascular endothelial growth factor, and MMP-2 were not modified in these conditions, the proteins released by proteolysis from the endothelial membrane intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and angiotensin-converting enzyme were increased (PϽ0.01). After blood stasis in varicose veins, the leukocyte markers lactoferrin, myeloperoxidase, and interleukin-8 were not modified, whereas L-selectin shed from leukocytes increased (PϽ0.05), and a major increase in pro-MMP-9, which is released from tertiary granules during polymorphonuclear activation, was observed (Pϭ0.0001). Conclusions-The

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Section: Discussionmentioning

confidence: 98%

mentioning

confidence: 99%

Plasma Matrix Metalloproteinase-9 as a Marker of Blood Stasis in Varicose Veins

et al. 2002

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“…Elevation of venous pressure activates inflammatory processes in the venous system including expression of E-selectin, ICAM-1 and VCAM-1 in the plasma obtained from leg veins of patients with and without varicose veins [118]. In another study, high venous pressure induced through venous occlusion with an inflated cuff elevated the expression of IL-1β, IL-6 and tumour necrosis factor-α in patients with and without varicose veins, and more so in the former [119,120].…”

Section: Alterations In Gene Expression With Stretch: Similarities Wimentioning

confidence: 99%

The Effect of Pressure-Induced Mechanical Stretch on Vascular Wall Differential Gene Expression

et al. 2012

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High blood pressure is responsible for the modulation of blood vessel morphology and function. Arterial hypertension is considered to play a significant role in atherosclerotic ischaemic heart disease, stroke and hypertensive nephropathy, whereas high venous pressure causes varicose vein formation and chronic venous insufficiency and contributes to vein bypass graft failure. Hypertension exerts differing injurious forces on the vessel wall, namely shear stress and circumferential stretch. Morphological and molecular changes in blood vessels ascribed to elevated pressure consist of endothelial damage, neointima formation, activation of inflammatory cascades, hypertrophy, migration and phenotypic changes in vascular smooth muscle cells, as well as extracellular matrix imbalances. Differential expression of genes encoding relevant factors including vascular endothelial growth factor, endothelin-1, interleukin-6, vascular cell adhesion molecule, intercellular adhesion molecule, matrix metalloproteinase-2 and -9 and plasminogen activator inhibitor-1 has been explored using ex vivo cellular or organ stretch models and in vivo experimental animal models. Identification of pertinent genes may unravel new therapeutic strategies to counter the effects of pressure-induced stretch on the vessel wall and hence minimise its notable complications.

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“…1,2 In addition, basic and clinical research have also demonstrated that upregulation of genes related to inflammation, such as tumor necrosis factor-␣, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1, to name a few, was observed in target organs and/or circulation of hypertensive animals and patients. [3][4][5][6] Increase in tissue and/or circulating levels of inflammatory cytokines suggest that the production of these cytokines increases the risk of plaque rapture.…”

mentioning

confidence: 99%

Is Vascular Endothelial Growth Factor a Missing Link Between Hypertension and Inflammation?

Morishita

2004

Hypertension

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Endothelial activation in patients with chronic venous disease

Cited by 83 publications

References 27 publications

Plasma Matrix Metalloproteinase-9 as a Marker of Blood Stasis in Varicose Veins

Plasma Matrix Metalloproteinase-9 as a Marker of Blood Stasis in Varicose Veins

The Effect of Pressure-Induced Mechanical Stretch on Vascular Wall Differential Gene Expression

Is Vascular Endothelial Growth Factor a Missing Link Between Hypertension and Inflammation?

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