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Results for “ETHINYL ESTRADIOL”

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At least 577 records · Page 32Linked to original sources
PubMed1976

[The course of total leukocytes and heparinocytes in the normal puerperium and during weaning under ethinyl estradiol sulfonate].

The inhibition of lactation by the depot oestrogen aethinyloestradiolsulfonate was accompanied by a delayed drop of the puerperal leukocytosis. Values of heparinocytes and Basophil-Age-Indices (BAI) were not significantly influenced. The reaction of the heparinocytes system is different in increasing classes of age. By depotoestrogens in the puerperium the princip of this reaction is not changed. Results don't support the hypothesis of influence of oestrogens upon puerperal and hormonal contraception risks of thromboembolism.

Basophils↗
PubMedDate not supplied

[The contraceptive efficacy and mechanism of action of combinations of ethinyl estradiol and norethisterone acetate].

The purpose of the study was to establish the optimal combinations of ethynilestradiol and norethysterone acetate exhibiting a high contraceptive activity. It was shown that the ratio of 1:20 (ethynilestradiol 0.04 mg/kg and norethysterone acetate 0.8 mg/kg) is characterized by a high contraceptive efficacy. The inhibitory effect on the incretion of lutropin and follitropin leading to the change of the process of oogenesis and gravidary reorganization of the endometrium underlies probably the mechanism of action.

Animals↗
PubMed1976

[Electron microscopic study on the proliferation and regression of the human endometrium following administration of a new depot estrogen ethinyl estradiol sulfonate].

The ultrastructure of endometrium was investigated after oral application of 1 or 3 mg of the new depot oestrogen etinyloestradiolsulfonate by means of long time observation with biopsies on postmenopause women. Details of this experimental proliferation was described. The highest functional activity in the endometrial gland and stromal cells was found 3 weeks after intake. There was no difference between ultrastructure following exogenous and endogenous oestrogen action. Degenerative changes within mitochondria were observed earlier than the regression in light microscopical picture.

Delayed-Action Preparations↗
PubMedDate not supplied

[Effect of ethinyl-estradiol on the biosynthesis and esterification of fatty acids in the rat liver].

Ethynyl-estradiol was shown to decrease the rate of biosynthesis of saturated, mono-, di-, tri- and tetraenic fatty acids in liver tissue and to increase the esterification of the newly synthesized fatty acids into triglycerides and phospholipids. The most distinct activation of esterification was found, if newly synthesized saturated fatty acids changed to triglycerides and tetraenic acids--into phospholipids. Ethynyl-estradiol stimulated also in liver tissue the esterification of exogenous saturated and unsaturated fatty acids into triglycerides and phospholipids, while relative esterification of unsaturated fatty acids into phospholipids tended to increase. The data obtained suggest that stimulation of endo- and exogenous fatty acids esterification into triglycerides and phospholipids of liver tissue may be important in pathogenesis of estrogen-induced hypertriglyceridemia.

Acetyl-CoA Carboxylase↗
PubMed1979

[Initial experience with ethinyl estradiol sulfonate (J 96) in the therapy of prostate carcinoma].

Ethinylestradiol sulphate (J 96) is a depot estrogen which in a dosage of 2 mg per week has clearly antigonadotropic effects and evokes a suppression of the free testosterone in bilaterally orchiectomized patients with carcinoma of the prostate. The good compatibility in oral application and the possibility for the controlled intake recommend its use for the long-term therapy of the carcinoma of the prostate.

Carcinoma↗
PubMed1975

[Effects of ethinyl estradiol compared with norethisterone (pure or contaminated) on vaginal keratinization of castrated rats].

Norethisterone samples are often contaminated by estrogen traces which can be measured by mass spectrometry and which invest the progestative with estrogenic properties in the Allen and Doisy test. Therefore, one had better, in pharmacodynamic experimenting, use samples that have been purified by chromatography or that are pure out of synthesis. However, one will not forget these are not without some estrogenicity, a fact which seems linked to the very nature of the norethisterone molecule.

Animals↗
PubMed1987

[Clinical study of ethinyl estradiol sulfonate in conservative therapy of prostate cancer].

Ethinylestradiol sulfonate is an orally applicable, potent depot estrogen with steroid structure. With a dosage of 2 mg per week it shows a distinct antigonadotropic and antiandrogenic effect. Its suitability for the hormone therapy of the carcinoma of the prostate is clinically and cytologically confirmed. It seldom has undesirable side effects. The oral application necessary only once a week guarantees a continuous supply of active substances with a good compliance by the patients.

Adenocarcinoma↗
PubMed1984

[Effect of sequential preparation with ethinyl estradiol sulfonate soft gelatin capsules and norethindrone acetate on carbohydrate metabolism].

An intravenous glucose tolerance test (i.v.GTT) was done before and after 6 months of using a sequential-type oral contraceptive in form of a weekly pill containing 0,6 mg ethinylestradiol-sulfonate (EES) soft gelatin capsules and 10 mg norethisterone acetate (NEA). 17 fertile, eumetabolic women are examined . There was no change neither average fasting blood glucose nor glucose assimilation after intake of ethinylestradiol. Basal as well as reactive insulin values increased by longer period of intake.

Adult↗
PubMedDate not supplied

Histometric and cytochitechral studies on the rat testis following combined administration of testosterone enanthate and ethinyl estradiol.

Combined administration of TE & EE for 72 days inhibited spermatogenesis. Testicular weight along with germinal height and tubular diameter decreased. Pachytene spermatocytes started becoming pycnotic and less in number by 24 days treatment. Almost no spermatozoa were seen in the lumen by 36 days and very few secondary spermatocytes and spermatids by 60 days. Marked disorganisation and desquamation was observed by the end of treatment. Leydig cells were also atrophied. Increase in swollen cell bodies, vacuolization, karyiolysis, pycnosis and cytolysis were observed after 72 days of treatment. Almost full recovery after 30 days of cessation of treatment was noticed.

Animals↗