In order to study changes in the calcium depots of the body during pregnancy and lactation, bone mineral deteminations were performed on fourteen pregnant women and eighteen mothers post partum by X-ray spectrophotomeyry. Pregnant women exhibited a loss in trabecular bone but not in cortical bone when measured once during late first or early second trimester and again one week post partum. Lactating women who nursed less than three months lost mineral during the first three months and than regained it while those who nursed for longer than three months had no losses during six months of study.
Isolated biopsy specimens of human peripheral arteries and veins, preincubated with 3H-(-)- noradrenaline (NA) to label the neural stores of NA, were used to study the Beta-adrenoceptors previously found to increase the secretion of 3H-NA evoked by electrical field stimulation of the adrenergic nerves of this tissue. The increase in nerve stimulation induced secretion of 3H-NA caused by 0.04 muM isoprenaline was prevented by 1 muM propranolol. This beta-blocking drug by itself slightly but significantly depressed the secretion of 3H-NA caused by nerve stimulation in the absence of isoprenaline. While the secretion of 3H-NA was not affected by known beta1-agonists, it was dose-dependently and reversibly increased by two different beta2-agonists. The effect of isoprenaline on 3H-NA secretion was not altered by a selective beta1-antagonist, but strongly reduced or abolished by a beta2-blocking drug. The results indicate that the beta-adrenoceptors involved in the control of NA secretion from the vasoconstrictor nerves of human omental blood vessels are only to a minimal extent stimulated by NA secreted from the nerves, and therefore do probably not mainly serve to mediate local positive feedback control of transmitter secretion; the receptors appear to be beta2 in nature.
Abstract.
Thyroxine-binding globulin (TBG), thyroxine-binding pre-albumin (TBPA), thyroxine (T4), free-T4, triiodothyronine (T3), and thyroid-stimulating hormone (TSH) were studied throughout apparently normal pregnancy in 290 cases grouped in 2 week intervals. TBG increased to a plateau level reached in the 24th week and was hereafter unchanged until term. T4 showed an increase until the 16th week of pregnancy and levelled off to a constant level for the rest of the pregnancy. Free-T4 declined to almost subnormal values for the non-pregnant state which was reached around the 20th week of pregnancy. T3 showed a slight and definite increase in the beginning of pregnancy and levelled off to a constant value after the 14th week. TSH increased towards the end of pregnancy also showing its maximum during the last 4 weeks. TBPA showed constant values throughout pregnancy. The results are discussed in view of the use of modern techniques and previously missing data in literature (TBPA).
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