The roles of turbulence and vasa vasorum in the aetiology of varicose veins

Crotty, T.P.

doi:10.1016/0306-9877(91)90063-5

Cited by 15 publications

(7 citation statements)

References 14 publications

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“…In the European population, 30–40% of adults are affected by this pathology [2]. Besides valvular incompetence and venous hypertension [3, 4], intrinsic abnormalities of the venous wall leading to dilatation with subsequent insufficiency contribute to the disease [5, 6, 7]. An abnormal distensibility of the venous wall characterizes the varicose veins.…”

Section: Introductionmentioning

confidence: 99%

Abnormal Deposition of Extracellular Matrix Proteins by Cultured Smooth Muscle Cells from Human Varicose Veins

Sansilvestri-Morel

Nonotte²,

Fournet-Bourguignon³

et al. 1998

J Vasc Res

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The aim of the present study was to verify whether the modifications of the extracellular matrix, described in varicose veins, are also present in cultures of smooth muscle cells from human varicose veins. The accumulation of collagen type III and fibronectin was determined by immunofluorescence in cultures of smooth muscle cells at passage 2–3 during the proliferation phase. After 5 days of culture, the immunostaining of both collagen type III and fibronectin was weaker in cells from varicose than in those of control veins while the expression of collagen type III and fibronectin messenger ribonucleic acids was not significantly different. Collagen type I and III synthesis were quantified by tritiated proline incorporation in control and varicose cell layers at postconfluence. Collagen type I deposition was similar in both types of cell layers while collagen type III was decreased in cell layers from varicose veins. Matrix metalloproteinases (MMPs) and their inhibitors (TIMPs) were also quantified by enzyme immunoassays in supernatants from smooth muscle cell cultures at postconfluence. No significant difference was observed in the synthesis of any of the MMPs (–1, –2 and –9) or their inhibitors (–1 and –2) tested. These data illustrate that smooth muscle cells cultured from varicose veins deposit less collagen type III and fibronectin than control cells despite comparable levels of mRNAs for these proteins suggesting dysregulation of posttranslational steps in the synthesis of both proteins by smooth muscle cells from varicose veins.

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Section: Introductionmentioning

confidence: 99%

Abnormal Deposition of Extracellular Matrix Proteins by Cultured Smooth Muscle Cells from Human Varicose Veins

Sansilvestri-Morel

Nonotte²,

Fournet-Bourguignon³

et al. 1998

J Vasc Res

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“…Activation of platelets and PMNs within venules can lead to the breakdown of the endothelial barrier function with serious pathophysiological consequences. The veins of the lower limbs are at particular risk in this context since their walls are rich in venules and since unfavourable hydrostatic conditions can cause backflow of venous blood [18] and of activated blood cells into these venules. Drugs, such as the flavonoid fraction in the red vine leaf extract AS 195, that protect and repair the venular endothelium appear to represent a very promising approach to the treatment of CVI.…”

Section: Discussionmentioning

confidence: 99%

“…These networks include abundant venules that − like tributuaries of a large river − feed their blood directly into the lumen of the parent vein. Under certain experimental circumstances backflow from the lumen of human saphenous veins to the microvasculature of their wall has been demonstrated [18]. It is conceivable that such unfavourable hydrostatic conditions may also occur during extended standing or sitting, especially so in a patient with incompetent valves.…”

Section: Abbreviationsmentioning

confidence: 99%

Protective Effects of Flavonoids Contained in the Red Vine Leaf on Venular Endothelium against the Attack of Activated Blood Components in vitro

Nees

Weiss

Reichenbach-Klinke

et al. 2011

Arzneimittelforschung

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New methods are described that allow the selective isolation of venular endothelial cells and their cultivation on porous filters to confluent monolayers. These filters with the attached endothelial cell layer can be mounted in a specially adapted apparatus allowing not only blood filtration studies, but now also the continuous registration of hydraulic conductivity (Lp) of tissue layers. This preparation responds dramatically to certain release products from simultaneously activated blood platelets and polymorphonuclear granulocytes (PMN) with a rise in Lp that, in situ, would lead rapidly to local oedema, arteriolar constriction and venular thrombosis. Selectively activated PMN alone induced only a modest increase in endothelial Lp that could be prevented by uric acid, an antioxidant. ASA prevented the activation of the blood cells, but not the effect of the release products per se, implying that the release products are probably eicosanoids. A standardized extract from red vine leaves (AS 195, active ingredient of Antistax Venenkapseln), containing in particular the flavonoids quercetin-3-O-beta-D-glucuronide and isoquercitrin (quercetin-3-O-beta-D-glucoside), not only prevented the deleterious effect of the release products on the venular endothelial monolayers but, applied promptly to an endothelium damaged by prior exposure to these release products, resulted in the repair of the endothelium. These findings identify for the first time the venular endothelium as a possible important therapeutic target in certain vascular diseases, chronic venous insufficiency being perhaps the most prominent example.

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“…30 On the contrary, increased levels of endogenous noradrenaline could be released from the vasa vasorum, dilating the vein by an overflow of adrenergic nerve activity. 31 The exact ratio of reduced secreted noradrenaline by the endothelium and the enhanced levels of endogenous noradrenaline of the vasa vasorum has not, however, been clearly understood. It is known, however, that low levels of noradrenaline have a constrictor tone on the vessel wall, although enhanced levels, as a result of increased volume reflux, could result in vasodilation.…”

Section: Changes Of the Endotheliummentioning

confidence: 99%

The Histopathology of Varicose Vein Disease

Somers

Knaapen

2006

Angiology

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Varicosity is a complex venous pathology affecting the lower extremities. The exact etiology and physiopathology of varicose vein disease remain, however, unclear. Several theories exist from incompetence of the valves to a disturbance of the smooth muscle cells (SMC) and extra-cellular matrix (ECM) organization providing a weakness of the venous wall. Multiple studies have been performed to explain the underlying mechanisms of varicosity inducing alterations in the expression patterns of the endothelium, SMC, and ECM. In that respect, most attention has been focused on the alteration of the endothelium due to blood stasis and hypoxia inducing migration/proliferation of the medial SMC into the intima. Also, studies in the deformation of the ECM induced by alterations of the expression patterns of the metalloproteinases (MMP) and their inhibitors (TIMPs) have been put forward to explain the etiology of varicosity. However, less attention has been paid to the hormonal changes that occur during pregnancy and menopause, crucial factors to be involved in the etiology of varicosity. Since alteration of the estrogen receptor-b (ERb) expression could enhance directly the cellular volume of SMC and thus the disorganization of the contractile-elastic units, hypertrophy of SMC must be accounted a pivotal role that could induce the weakness of the venous wall. Altogether, this review summarizes an overview of the latest findings of varicosity with respect to the histopathological changes of the different cellular components of the varicose vein wall related to functional and morphologic alterations.

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The roles of turbulence and vasa vasorum in the aetiology of varicose veins

Cited by 15 publications

References 14 publications

Abnormal Deposition of Extracellular Matrix Proteins by Cultured Smooth Muscle Cells from Human Varicose Veins

Abnormal Deposition of Extracellular Matrix Proteins by Cultured Smooth Muscle Cells from Human Varicose Veins

Protective Effects of Flavonoids Contained in the Red Vine Leaf on Venular Endothelium against the Attack of Activated Blood Components in vitro

The Histopathology of Varicose Vein Disease

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