varicose veins/hypoxia

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Perfused human saphenous veins for the study of the origin of varicose veins: role of the endothelium and of hypoxia.

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If venous stasis due to blood stagnation has been recognized to be involved in the development of varicose veins, the mechanism linking this situation to the modifications of the venous wall observed in varicoses is still unclear. In order to study this mechanism, human saphenous veins were

Increased expression of hypoxia-inducible factor-1α and metallothionein in varicocele and varicose veins.

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OBJECTIVE The increased blood stasis and venous volume pressure causing tissue hypoxia are observed in both varicocele and varicose veins. Metallothionein (MT), a metal-binding protein, protects against cell apoptosis under hypoxic stress. It also plays an important role in collateral flow recovery

Increased expression of hypoxia-inducible factor-1alpha and Bcl-2 in varicocele and varicose veins.

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BACKGROUND Primary vein wall abnormalities leading to secondary blood stasis and increased venous pressure that cause tissue hypoxia are observed in varicocele and varicose veins. Both types of diseased vessels are characterized by dilated thickened vein walls. Hypoxia upregulates Bcl-2

Pathogenic mechanisms in varicose vein disease: the role of hypoxia and inflammation.

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OBJECTIVE Although the aetiology of varicose veins remains unknown, recent studies have focused on endothelial cell integrity and function. Among the regulatory factors of vessel tone, synthesises, pro- and anti-inflammatory, adhesion molecules and the transcription factor hypoxia inducible factor-1

Increased activation of the hypoxia-inducible factor pathway in varicose veins.

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BACKGROUND Venous hypoxia has been postulated to contribute to varicose vein (VV) formation. Direct measurements of vein wall oxygen tension have previously demonstrated that the average minimum oxygen tensions were significantly lower in VVs compared with non-varicose veins (NVVs).

Venous hypoxia: a poorly studied etiological factor of varicose veins.

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Venous hypoxia has long been postulated as a potential cause of varicosity formation. This article aimed to review the development of this hypothesis, including evidence supporting and controversies surrounding it. Vein wall oxygenation is achieved by oxygen diffusing from luminal blood and vasa

Involved intrinsic apoptotic pathway in the varicocele and varicose veins.

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BACKGROUND Disordered programmed cell death may play a role in the development of venous diseases. Tissue hypoxia caused by blood stagnation and venous hypertension is the similar etiology of varicocele and varicose veins. We studied the vascular histopathology and determined whether there is the

Cyanoacrylate in the treatment of gastric varices complicated by multiple pulmonary emboli.

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Bleeding gastric varices are increasingly being obliterated with the aid of endoscopic injection of n-butyl-cyanoacrylate (histoacryl) diluted with lipiodol. This glue acts as a tissue adhesive that polymerizes on contact with blood in a gastric varix. Severe glue pulmonary embolism is a rare

Histopathological changes in venous grafts and in varicose and non-varicose veins.

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OBJECTIVE To examine veins histologically from different sites in the body to study the effect of venous pressure; and to examine veins used as aortocoronary grafts. METHODS The axillary vein, femoral vein at the inguinal ligament, the short saphenous vein at the knee and the long saphenous vein at

Interactions between endothelial cells and smooth muscle cells after their activation by hypoxia. A possible etiology for venous disease.

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Because of their localization at the interface between blood and tissue, endothelial cells are responsible for the maintenance of vascular homeostasis. They fulfil a series of various functions and constantly interact with circulating leukocytes and with the smooth muscle cells (SMC) present in the

Upregulation of the gene expression of CLOCK is correlated with hypoxia-inducible factor 1α in advanced varicose lesions.

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According to previous literature, venous hypoxia and the hypoxia‑inducible factor (HIF) pathway may contribute to the pathogenesis of varicose veins (VVs). It is widely accepted that the circadian locomotor output cycles kaput (CLOCK) gene affects nucleotide excision repair, DNA damage checkpoints

Histomorphological and pathobiochemical changes of varicose veins. A possible explanation of the development of varicosis.

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The authors should like to contribute to the unsettled problem of the development of varicose venous disease with their own experience. They evaluate parallel the histomorphological observations and certain pathobiochemical changes which can be recognized in exstirpated varicose veins. Fourty five

Temporary deterioration of pulmonary functions after injection sclerotherapy for cirrhotic patients with esophageal varices.

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In 34 cirrhotic patients with esophageal varices, a significant but temporary deterioration in pulmonary function tests occurred 24 h after endoscopic injection sclerotherapy using 5% ethanolamine oleate. Included were vital capacity, forced expiratory volume in 1 s, closing volume/vital capacity

Role of the endothelium and blood stasis in the development of varicose veins.

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Today, chronic venous insufficiency affects millions of people but the investigation of veins and of venous diseases is still very poor. Additionally, the mechanism of the occurrence of varicose veins is not understood. Blood stasis is often associated with these pathological situations and we

[Pulmonary embolism after endoscopic injection with N-butyl-2-cyanoacrylate for gastric varices].

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Gastric varices occur in one-third of patients with portal hypertension. Bleeding from gastric varices remains a significant cause of death. Currently the first-line of treatment for gastric varices is endoscopic obliteration with N-butyl-2-cyanoacrylate. Though relatively safe, this option has

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