Leukocyte activity in the microcirculation of the leg in patients with chronic venous disease

Saharay, M.; Shields, D. A.; Porter, John B.; Scurr, J. H.; Smith, Philip

doi:10.1016/s0741-5214(97)70188-5

Cited by 98 publications

(54 citation statements)

References 22 publications

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“…During rolling leukocytes attach loosely to the endothelium by a L-selectins and E-selectins, which tether leukocytes to the endothelial cells [44]. Leukocytes tumbles end-over-end along the endothelium.…”

Section: Molecular Mechanisms Involved In the Inflammatory Processmentioning

confidence: 99%

The inflammatory reaction during chronic venous disease of lower limbs.

Ojdana

Safiejko²,

Lipska³

et al. 2009

Folia Histochem Cytobiol.

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Chronic venous disease (CVD) is an insufficiency of distal veins caused by their partial or total obstruction, endothelial distension and functional disorders. Chronic venous disease of lower limbs is common problem and affects millions of people. In this article we suggest that inflammatory process is involved in the structural remodeling in venous valves and in the venous wall, leading to valvular incompetence and the development of varicose veins.

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Section: Molecular Mechanisms Involved In the Inflammatory Processmentioning

confidence: 99%

The inflammatory reaction during chronic venous disease of lower limbs.

Ojdana

Safiejko²,

Lipska³

et al. 2009

Folia Histochem Cytobiol.

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“…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.…”

mentioning

confidence: 99%

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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“…Several studies show enhanced infiltration of lymphocytes, monocytes, macrophages and neutrophils into venous wall [32]. Inflammatory cells may release proteolityc enzymes, free radicals and cytokines responsible for the destruction of tissue [47,48].…”

Section: Discussionmentioning

confidence: 99%

“…The interaction of integrins and Ig-superfamily adhesion molecules causes firm adhesion of leukocytes to the endothelial cells and their migration through the endothelium [37]. Activated leukocytes migrate into venous wall and venous valve [38]. Leukocytes during the inflammatory process generate numerous substances (e.g.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of the memory CD4+ and CD8+ T cells homeostasis during chronic venous disease of lower limbs.

Ojdana

Safiejko²,

Milewski³

et al. 2010

Folia Histochem Cytobiol.

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More and more is known about the role of venous wall abnormalities and valvular incompetence in the development of chronic venous disorders (CVD). Unfortunately detailed mechanisms of CVD pathophysiology are not well understood. Recent studies focus on involvement of the inflammatory process in the structural remodeling of venous valvues and venous wall. The aim of this study is to investigate and to document the memory T cells homeostasis in CVD patients. In this study we present lymphocytic changes in blood from varicose veins in terms of total CD4+ and CD8+ T cells and their particular subsets of memory T cells: T N , T CM and T EM . Results suggest that immunological memory may be involved in the CVD development.

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Leukocyte activity in the microcirculation of the leg in patients with chronic venous disease

Cited by 98 publications

References 22 publications

The inflammatory reaction during chronic venous disease of lower limbs.

The inflammatory reaction during chronic venous disease of lower limbs.

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

Evaluation of the memory CD4+ and CD8+ T cells homeostasis during chronic venous disease of lower limbs.

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