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• W1499687897 abstract "Abstract Estrogen therapy has been used clinically as a hemostatic adjuvant in various hemorrhagic disorders. Preference has been given to a water soluble conjugated estrogen preparation, which can be injected intravenously. The mechanism of the hemostatic action of estrogens, which would support the encouraging clinical results, has not yet been elucidated. Studies with estrogens on intravascular clotting have given equivocal results. Estrogen administration in animal experiments increases the blood level of Factor V and prothrombin and depresses antithrombin activity. Furthermore, it appears to reverse abnormal platelet and megakaryocyte morphology. Clinical observations have suggested that there is a relationship between the level of circulating estrogens and capillary resistance. A drop of the estrogen level, a physiological change in certain periods of a woman's life, results in capillary fragility and a bleeding tendency. Estrogen administration to women during menses and menopause or to patients with ovarian dysfunction abolishes hot flushes, reverses the abnormal capillary fragility, and the bleeding tendency. The morphological basis of capillary fragility and permeability is not well established. It is not clear what is the correlation between capillary permeability and capillary fragility and on the one hand, vascular contraction, endothelial swelling, changes of the subendothelial and pericapillary matrix, and capillary stickiness, on the other hand. Recent histochemical studies have shown that estrogens may increase the formation and polymerization of vascular acid mucopolysaccharides. This change has been regarded as a morphological basis of capillary strength and it has been suggested that the hemostatic action of estrogens may be mediated mostly by influencing vascular reactions. The functional role of vascular mucopolysaccharides in hemostasis has been recently investigated. Some of the vascular mucopolysaccharide fractions may participate in the coagulation mechanism, but they appear to have also anticoagulant effect. All these data indicate that neither the simple accumulation of intimal acid mucopolysaccharides, nor the metachromasia observed following estrogen administration explains the hemostatic effect of this hormone. Further careful studies are still required to reveal how estrogens promote hemostasis and what the significance of the accumulation of acid mucopolysaccharides is in this mechanism. The connection between the administration of oral contraceptives and thromboembolism remains unresolved because of the paucity of basic biological data. Although there is no evidence that the administration of either estrogen or progestrone, alone, predisposes to thrombosis, the effect of synthetic gestogens or of a combination of estrogen and progesterone has not been determined and may be different. The presently reported experimental and clinical studies with estrogen may serve as a model for basic investigation of the gestogens." @default.
• W1499687897 created "2016-06-24" @default.
• W1499687897 creator A5061907641 @default.
• W1499687897 date "1963-10-01" @default.
• W1499687897 modified "2023-09-23" @default.
• W1499687897 title "The role of vascular mucopolysaccharides in the hemostatic action of estrogens" @default.
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