beta-escin and Hypertension

beta-escin has been researched along with Hypertension* in 4 studies

Trials

3 trial(s) available for beta-escin and Hypertension

ArticleYear
Microvascular changes in venous hypertension due to varicose veins after standardized application of Essaven gel--a placebo-controlled, randomized study.
    Angiology, 2001, Volume: 52 Suppl 3

    The involvement of the microvascular structure in chronic venous insufficiency (CVI) causes venous hypertensive microangiopathy (VHM), which leads to venous ulceration. VHM is characterized by enlarged and ramified capillaries, increased flux and capillary permeability, edema, and altered function of microlymphatics. TcPO2 is decreased and CO2 increased. This perfusional paradox is caused by hyperperfusion in the deep skin layers with hypoperfusion of superficial nutritional capillaries. Exchanges in the capillary bed are altered. Nutritional skin alterations eventually lead to venous ulceration. Edema is the consequence of increased capillary pressure, reduced clearance, and by an increased exchange surface of capillaries. The aim of this randomized, placebo-controlled study was to evaluate the effect of local treatment with Essaven gel (EG) in 22 subjects with VHM due to severe varicose veins, treated with a single application. Measurements of flux, PO2 and PCO2 in standardized conditions of application indicated a significant decrease of the abnormally increased flux and CO2; PO2 increased in the treatment group. Essaven gel, in comparison with placebo and controls acutely improves the microcirculation in VHM even with a single application.

    Topics: Administration, Topical; Adult; Double-Blind Method; Drug Combinations; Escin; Female; Fibrinolytic Agents; Heparin; Humans; Hypertension; Male; Microcirculation; Middle Aged; Phospholipids; Skin; Varicose Veins

2001
Changes in microcirculation in venous ulcers with Essaven gel--a pilot, cross-over, placebo-controlled, randomized study.
    Angiology, 2001, Volume: 52 Suppl 3

    Microcirculatory changes in chronic venous insufficiency (CVI) due to venous hypertension produce venous hypertensive microangiopathy (VHM) and lead to ulceration. VHM is characterized by enlarged, convoluted capillaries; increase in flux, permeability, and edema; and altered microlymphatics. PO2 is decreased and CO2 increased. Capillary exchanges are altered and nutritional alterations in association with microtrauma may cause venous ulcers. The aim of this pilot, cross-over, randomized, placebo-controlled study was to evaluate the effect of local treatment with Essaven gel (EG) (single acute application) in 10 subjects with VHM and venous ulcers. The study was structured over 3 days: day 1 was used for the control evaluation for all patients. One group was randomized for the sequence placebo (day 2) and EG the following day; the second group with the sequence EG (day 2) and placebo (day 3). Independently from the sequence, measurements of flux and PO2 in standard conditions showed positive changes (significant decrease of the abnormally increased flux, PO2 increase) in the EG treatment group. Changes in the placebo group were limited and associated with skin manipulation. In conclusion, EG acutely improves microcirculation in limbs with VHM and ulceration even with a single application.

    Topics: Administration, Topical; Cross-Over Studies; Drug Combinations; Escin; Female; Fibrinolytic Agents; Heparin; Humans; Hypertension; Male; Microcirculation; Middle Aged; Phospholipids; Pilot Projects; Treatment Outcome; Varicose Ulcer

2001
Microangiopathy and venous ulceration: topical treatment with Essaven gel--a placebo-controlled, randomized study.
    Angiology, 2001, Volume: 52 Suppl 3

    The involvement of the microcirculation in chronic venous insufficiency (CVI) due to venous hypertension causes venous hypertensive microangiopathy (VHM) and venous ulceration. VHM is characterized by the presence of enlarged convoluted capillaries; microvascular thrombosis with obliteration of some capillaries; increase in flux, permeability, and edema; and altered function of microlymphatics. PO2 is decreased and CO2 increased. Capillary exchanges are altered, and nutritional alterations eventually lead to venous ulcers. Edema is associated with increased capillary pressure, reduced clearance, and an increased exchange surface of capillaries, which become tortuous and glomerular-like. The aim of this randomized, placebo-controlled study was to evaluate the effect of local treatment with Essaven gel (EG) in 28 subjects with venous microangiopathy due to severe CVI and ulcers treated with a single acute application, Measurements of laser Doppler flux, PO2 and PCO2 in standardized conditions of application showed positive microcirculatory changes (significant decrease of the abnormally increased flux and CO2 while PO2 increased) in the EG treatment group. Changes in the placebo and control group were more limited (changes in the placebo group were mainly associated with skin manipulation when placebo-EG was applied). In conclusion, Essaven gel, in comparison with placebo, acutely improves the microcirculation in VHM even with a single application.

    Topics: Administration, Topical; Adult; Aged; Double-Blind Method; Drug Combinations; Escin; Female; Fibrinolytic Agents; Heparin; Humans; Hypertension; Male; Microcirculation; Middle Aged; Peripheral Vascular Diseases; Phospholipids; Varicose Ulcer; Venous Insufficiency

2001

Other Studies

1 other study(ies) available for beta-escin and Hypertension

ArticleYear
Augmented agonist-induced Ca(2+)-sensitization of coronary artery contraction in genetically hypertensive rats. Evidence for altered signal transduction in the coronary smooth muscle cells.
    The Journal of clinical investigation, 1994, Volume: 94, Issue:4

    The Ca2+ responsiveness of vascular smooth muscle myofilaments is not unique: it is increased during neuro-humoral activation and decreased during beta-adrenergic stimulation. In this study we tested whether an augmented Ca2+ responsiveness of smooth muscle myofilaments may contribute to the increased coronary tone observed in hypertension using beta-escin-permeabilized coronary arteries from 3-mo-old stroke-prone spontaneously hypertensive rats (SHRSP) and their age matched normotensive reference strain (WKY rats). In intact coronary arteries, the response to 5-hydroxytryptamine (5-HT) but not to KCl was larger in SHRSP than in WKY rats. In beta-escin permeabilized coronary arteries in which the receptor effector coupling is still intact, 5-HT enhanced force at constant submaximal (Ca2+) (pCa 6.38) to a greater extent in SHRSP. The Ca2+ sensitizing effect of 5-HT was mimicked by GTP gamma S (0.01-10 microM); again this effect was larger in SHRSP. In the absence of 5-HT or GTP gamma S the Ca2+ force relation was similar in both groups. Forskolin induced relaxation at constant submaximal (Ca2+). This desensitizing effect was smaller in SHRSP than in WKY rats. In conclusion, this study shows that intracellular signalling pathways involved in modulating the Ca2+ responsiveness of coronary smooth muscle myofilaments are altered in the genetically hypertensive animals favoring a hypercontractile state in the coronary circulation.

    Topics: Actin Cytoskeleton; Animals; Calcium; Cell Membrane Permeability; Colforsin; Coronary Vessels; Escin; Guanosine 5'-O-(3-Thiotriphosphate); Hypertension; In Vitro Techniques; Male; Muscle Contraction; Muscle, Smooth, Vascular; Potassium Chloride; Rats; Rats, Inbred SHR; Rats, Inbred WKY; Serotonin; Signal Transduction

1994