elastin and Thrombophlebitis

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 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 stripped saphenas have been studied. They were divided into two groups: a macroscopically normal and a varicose one. The varicose patients were divided again into two subsamples according to the occurrence or lack of thrombophlebitis in their medical case history. The authors were looking for the appropriate pathobiochemical changes of the vessel walls running parallel to the usual histopathological changes. It seems quite possible that the effect which triggers the development of the disease could be anything which causes hypoxia, alters the energy metabolism of the otherwise bradytrophic vascular tissues. Accumulation of proteoglycans, as well as collagen and elastic fibers in place of the smooth muscle cells may cause a decrease in the elasticity of the veins and may produce favourable conditions to thrombus formation and local inflammation.

Topics: Carbon Dioxide; Collagen; Elastin; Electron Transport Complex IV; Female; Humans; Lactates; Lactic Acid; Male; Middle Aged; Proteoglycans; Saphenous Vein; Thrombophlebitis; Thromboxane A2; Tissue Plasminogen Activator; Varicose Veins

Topics: Animals; Anticoagulants; Basement Membrane; Blood Flow Velocity; Blood Vessels; Collagen; Connective Tissue; Elastin; Endothelium; Endotoxins; Epithelial Cells; Epithelium; Humans; Microscopy, Electron; Platelet Adhesiveness; Rabbits; Thrombophlebitis; Thrombosis