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Biomedical subjects

O Bellmann

Publications and source records attributed to O Bellmann.

At least 55 records · Page 3Linked to original sources
PubMed1976

Studies of the kinetics and metabolism of 17 beta-heptanoyl-17 alpha-ethinyl-4-oestren-3-one-7-3H (norethisterone enanthate) in humans following intramuscular injection.

The kinetics and metabolism of 17 beta-heptanoyl-17 alpha-ethinyl-4-oestren-3-one-7-3H (7-3H-norethisterone enanthate, NET-En) after i.m. injection in two female subjects is described. 177.4 mg and 174.5 mg NET-En were injected. Maximum 3H-activity in plasma was reached 8 to 14 days after the injection. In terms of NET-En it amounted to 70-100 mug/100 ml. Maximum NET concentration was reached on the 4th to 8th day and amounted to about 1 mug/100 ml. After 4 weeks NET concentration was still about 0.05 to 0.1 mug/100 ml and even after 6 weeks NET was still detectable in plasma. In 14 days the two subjects excreted about 13% of the administered dose in the urine and about 15% and 21%, respectively, in the faeces. On the basis of a rough calculation, the subjects eliminated about 60% and 55% of the radioactivity with urine and faeces within 42 days.

Female↗
PubMed1976

[Hormonal regulation of lactation (author's transl)].

Lactation is controlled by hormones from several endocrine glands. An undisturbed function of the anterior pituitary, of the adrenals, and of the ovaries is a prerequisite for a normal morphogenesis of the mammary gland. The epithelial ducts proliferative under the combined influence of estrogens, glucocorticoids and growth hormone, whereas the lobuloalveolar development depends on progesterone and prolactin in addition to the fore-mentioned hormones. During pregnancy pituitary prolactin may be substituted by placental lactogen. Milk synthesis begins in the second half of pregnancy. It is supported by prolactin and cortisol, which directly act on enzyme activities and processes of differentiation of the alveolar cells. The sudden surge in the secretion of milk after parturition is most likely due to the rapid decline of the serum levels of progesterone. The ejection of milk from the lactating mammary gland is controlled by a neuroendocrine reflex mechanism. Suckling is the appropriate stimulus for the release of oxytocin from the posterior pituitary. Oxytocin increases intramammary pressure by inducing contraction of the myoepithelial cells and thus aids in expelling the milk from the mammary glands. Maintenance of normal postpartum lactation depends on frequent and intensive suckling. Suckling does not only stimulate the release of oxytocin, but also provokes secretion of prolactin and ACTH. This increase in prolactin caused by suckling guarantees galactopoesis. Influencing secretion of prolactin has been proven to be a useful tool for regulating lactation. The experimental ergot derivative 2-Brom-alpha-ergocryptine is a potent suppressor of prolactin secretion from the anterior pituitary. In contrast to estrogens, alone or in combination with progestagens or androgens, this drug is not only effective in suppressing the onset of lactation, but also in inhibiting lactation once milk secretion had started. As to stimulating lactation in the human there is no effective drug available up to now.

Adrenocorticotropic Hormone↗
PubMed1975

Influence of pregnancy on the kinetics of insulin.

The disappearance rate of intravenously injected insulin was investigated in the serum of 30 women during the third trimester of pregnancy and 6 to 8 weeks post partum, in order to determine whether pregnancy has an influence on insulin kinetics in human subjects. Both women with unimpaired glucose tolerance and those with latent diabetes were included in this study. The disappearance rate of exogenous serum insulin in pregnancy was characterized by a two-compartment model. Multivariate analyses of variance were used to determine whether the estimated parameters of this model during pregnancy differ from those obtained after the puerperium and whether the insulin kinetics are altered when carbohydrate metabolism is disturbed. The kinetics of insulin during pregnancy did not differ from those after pregnancy. Thus, hyperinsulinemia observed in pregnancy cannot be explained by a change in the insulin kinetics. It appears improbable that the insulin-degrading enzyme activities of the placenta participate in degradation of insulin circulating in the maternal blood. A connection between the decline of glucose tolerance during pregnancy and the kinetics of exogenous insulin could not be found.

Adult↗