Topic
Hydroxyethylrutoside
About: Hydroxyethylrutoside is a research topic. Over the lifetime, 6 publications have been published within this topic receiving 293 citations. The topic is also known as: hydroxyethylrutosides & oxerutins.
Papers
TL;DR: While its role in diabetic retinopathy and haemorrhoids requires some clarification, hydroxyethylrutosides therapy shows promise as a useful additional option for the management of oedema and other symptoms of chronic venous insufficiency.
Abstract: Hydroxyethylrutosides is a standardised mixture of semisynthetic flavonoids, mainly mono-, di-, tri-, and tetrahydroxyethylrutosides, which acts primarily on the microvascular endothelium to reduce hyperpermeability and oedema. In patients with chronic venous insufficiency or diabetes, hydroxyethylrutosides improves microvascular perfusion and microcirculation, and reduces erythrocyte aggregation. The preparation also has a possible protective effect on the vascular endothelium. In short to medium term placebo-controlled studies (up to 6 months) hydroxyethylrutosides therapy improved signs and symptoms of chronic venous insufficiency, including venous insufficiency associated with pregnancy and lymphoedema, and was well tolerated. However, the long term effects of hydroxyethylrutosides administration have yet to be demonstrated. The preparation also alleviated symptoms in patients with severe haemorrhoids, although there were no corresponding objective improvements. Hydroxyethylrutosides administration has been associated with reductions in retinal vascular permeability in patients with diabetic retinopathy but has no apparent effect on signs of retinal haemorrhage, although a reduction in oedema and haemorrhage has been reported in other patients receiving oral hydroxyethylrutosides in the acute phase of central retinal vein occlusion. There are only limited effective pharmacological treatment options for patients with chronic venous insufficiency or lymphoedema, and hydroxyethylrutosides clearly improves signs and symptoms of these disorders. While its role in diabetic retinopathy and haemorrhoids requires some clarification, hydroxyethylrutosides therapy shows promise as a useful additional option for the management of oedema and other symptoms of chronic venous insufficiency.
93 citations
TL;DR: In a group of volunteers, smoking two cigarettes produced a significant increase in the number of circulating endothelial cells, and this effect was suppressed in another group by a preventive oral administration of a hydroxyethylrutoside preparation.
Abstract: In a group of volunteers, smoking two cigarettes produced a significant increase in the number of circulating endothelial cells. This effect was suppressed in another group by a preventive oral administration of a hydroxyethylrutoside preparation. The results fully confirmed our earlier experimental findings in rats.
37 citations
Journal Article•
TL;DR: O-(beta-Hydroxyethyl)-rutoside administration was found to effectively block the renal injury without interfering with the antitumor efficacy of the combined regimen of WBH-cisplatin therapeutic regimen.
Abstract: A bioflavonoid, o-(beta-hydroxyethyl)-rutoside, has been investigated for its potential to increase the therapeutic index of the combined treatment modalities of whole body hypothermia (WBH) (41.5 degrees C) and chemotherapy (cisplatin) in studies utilizing a transplantable fibrosarcoma solid tumor model in Fischer rats. When whole body WBH was induced 45 min after cisplatin administration, a significantly increased tumor growth delay was noted beyond that achieved by either treatment modality alone. The combination of WBH and cisplatin treatments, however, produced an unacceptable increase in renal injury. o-(beta-Hydroxyethyl)-rutoside administration was found to effectively block the renal injury without interfering with the antitumor efficacy of the combined regimen. Potential explanations for the ability of o-(beta-hydroxyethyl)-rutoside to affect the increase in WBH-cisplatin therapeutic regimen are discussed.
22 citations
Journal Article•
TL;DR: Observations on urinary excretion in man are compatible with the finding in experimental animals that the major route of hydroxyethylrutoside excretion is via the biliary-enteric route.
Abstract: 1. following oral administration of a [14C]-hydroxyethylrutoside (Paroven, Venoruton) preparation (HR) to three subjects, 3.05--5.97% of the administered [14C] was excreted in urine. Unchanged urinary [14C]-hydroxyethylrutosides represented 1.57--1.96% of the total dose. 2. Significant levels of [14C] were detected in plasma within 1 h of oral administration of HR. Peak levels were observed from 2--9 h. 3. The presence in urine of [14C]-3',4',5,7-tetra-O-(beta-hydroxyethyl)rutoside, [14C]-3',4',7-tri-O-(beta-hydroxyethyl)rutoside and [14C]-4',7-di-O-(beta-hydroxyethyl)rutoside was shown by radioscanning and/or spectal methods. 4. Administration of a second oral dose of [14C]-HR to each of the three subjects following extended dosage of nonlabelled HR did not result in any increase in urinary [14C] excretion over that observed after administration of a single oral dose. 5. Observations on urinary excretion in man are compatible with the finding in experimental animals that the major route of hydroxyethylrutoside excretion is via the biliary-enteric route.
14 citations
TL;DR: It is suggested that a possible explanation for the improvement in venous insufficiency by HR observed clinically could be their ability to inhibit the activation of endothelial cells during blood stasis.
Abstract: 1. A clinically available mixture of hydroxyethylrutosides (HR) was examined as inhibitors of endothelial cell activation by hypoxia in vitro. Thus, the effects of HR on ATP depletion, phospholipase A2 activation and neutrophil adherence were investigated in hypoxia-activated human umbilical vein endothelial cells in primary cell culture. 2. Our results show that HR inhibited two important steps of the activation of endothelial cells by hypoxia: the decrease in ATP content, which is the starting point of the process, and the activation of phospholipase A2 one enzyme responsible for the release of inflammatory mediators. This inhibition was dose-dependent with 70 to 90% inhibition at 500 micrograms ml-1 of HR. 3. In addition, hypoxia-activated endothelial cells increased their adhesiveness for neutrophils. This process could also be prevented in a dose-dependent manner if endothelial cells were incubated in the presence of HR. This inhibition was confirmed by a morphological study. 4. In conclusion, the results of this study suggest that a possible explanation for the improvement in venous insufficiency by HR observed clinically could be their ability to inhibit the activation of endothelial cells during blood stasis.
13 citations
Related Topics (5)
Performance Metrics
| Year | Papers |
|---|---|
| 2011 | 1 |
| 1996 | 1 |
| 1992 | 1 |
| 1988 | 1 |
| 1979 | 1 |
| 1976 | 1 |