elastin and Venous-Insufficiency

Epidemiological data suggested an involvement of the progestogen component in the pathomechanism of venous and arterial diseases during intake of oral contraceptives. The influence of progestogens on haemostasis parameters depend on type and dose of the progestogen, the presence of an estrogen, the route of application, and the duration of use. Treatment of women with progestogen-only preparations caused only minor effects on coagulation and fibrinolysis. Similarly, during hormone replacement therapy with natural estrogens, the additional application of progestogens induced no unfavourable changes on haemostasis. In contrast, the use of ovulation inhibitors resulted in an acceleration of coagulation and fibrinolysis. This is primarily induced by the marked action of ethinylestradiol on hepatic and vascular function. Progestogens with androgenic properties may counteract the estrogen-induced changes in the hepatic synthesis of platelet aggregation and readiness for coagulation. Estrogen and progesterone receptors are localized in endothelial and smooth muscle cells of the vessel wall, but there are differences in the response of veins and arteries to sex steroids. Estrogens and progestogens may influence collagen and elastin synthesis, and the release of vasoactive compounds and of factors controlling fibrinolysis from endothelium. In veins, progestogens may increase distensibility and capacitance resulting in a decreased blood flow. In predisposed women, this may lead to venous stasis and thrombosis. In arteries, progestogens may act as vasoconstrictors, and may enhance vasospasms at sites of injured endothelium which finally may lead to ischemic diseases.

Topics: Arteries; Blood Circulation; Blood Coagulation; Collagen; Contraceptives, Oral; Elastin; Endothelium, Vascular; Estradiol Congeners; Estrogen Replacement Therapy; Estrogens; Ethinyl Estradiol; Female; Fibrinolysis; Hemostasis; Humans; Liver; Muscle, Smooth, Vascular; Ovulation; Platelet Aggregation; Progestins; Receptors, Estrogen; Receptors, Progesterone; Thrombophlebitis; Vascular Capacitance; Vascular Diseases; Veins; Venous Insufficiency

The passive properties of the venous wall are important for the compliance function of the venous system. The objective of this study was to quantify the passive biomechanical response and structural growth and remodeling of veins subjected to chronic venous reflux and hypertension.. To investigate the effects of venous reflux on venous mechanics, the tricuspid valve was injured in a canine model by disrupting the chordae tendineae. The conventional inflation-extension protocol in conjunction with intravascular ultrasound was used to investigate the passive biomechanical response of both control common iliac veins (n = 9 dogs) and common iliac veins subjected to 8 weeks of venous reflux and hypertension (n = 9 dogs). The changes in vein wall thickness and constituent composition were quantified by multiphoton microscopy and histologic evaluation.. Biomechanical results indicate that the veins became less compliant when exposed to 8 weeks of chronic venous reflux and hypertension. The mechanical stiffening was found to be associated with a significant increase in wall thickness (P < .05) and collagen-to-elastin ratio (P < .05). After 8 weeks of chronic reflux and hypertension, the circumferential vein wall stress was significantly reduced (P < .05) because of wall thickening, although it was not restored to control levels.. The growth and remodeling of the venous wall reduces the wall stress, but the stress remains higher than at baseline at 8 weeks. The compliance of the veins also decreases because of the increase in wall thickness and remodeling of the microstructure of the venous wall. These findings provide insight into potential adaptations of the venous system in reflux and hypertension.

Topics: Animals; Collagen; Compliance; Disease Models, Animal; Dogs; Elastin; Femoral Vein; Hypertension; Iliac Vein; Stress, Mechanical; Venous Insufficiency

Varicose veins may be due to weakness of the vein wall as a result of structural problems. There are conflicting findings in the literature about these problems especially concerning collagen, elastin and smooth muscle cells content. The aim of this study was to look at the structural abnormalities of varicose veins (with and without valvular incompetence).. We studied 70 specimens of long saphenous veins from 35 patients (24 with varicose and 11 with normal veins). Two specimens were taken from each vein approximately 3-4 cm from the saphenofemoral junction. Vein specimens were processed for histological and electron microscopic studies. Both qualitative and quantitative analyses were performed to assess the degree of wall changes. Using the image analyzer, contents of collagen, elastin and smooth muscle cells, in addition to intimal and medial thickness, were measured.. Light microscopy revealed significant increase in intimal and medial thickness and collagen content of media and significant decrease in elastin content in varicose veins compared with normal veins. There was no statistical significant difference between varicose veins with and without saphenofemoral valve incompetence. Electron microscopy showed marked degenerative changes in intima and media of varicose veins.. The findings in our study supported the theory of primary weakness of the vein wall as a cause of varicosity. This weakness is due to intimal changes, disturbance in the connective tissue components and smooth muscle cells.

Topics: Adult; Case-Control Studies; Collagen; Egypt; Elasticity; Elastin; Female; Humans; Male; Microscopy, Electron; Myocytes, Smooth Muscle; Saphenous Vein; Saudi Arabia; Staining and Labeling; Tunica Intima; Tunica Media; Varicose Veins; Venous Insufficiency

Topics: Collagen; Elasticity; Elastin; Humans; Microscopy, Electron; Myocytes, Smooth Muscle; Saphenous Vein; Staining and Labeling; Tunica Intima; Tunica Media; Varicose Veins; Venous Insufficiency