Biomedical subjects
Publications and source records attributed to P Eneroth.
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Rat growth hormone (rGH) (100 micrograms/kg) produced 2-4 h after its i.v. injection a rapid reduction of catecholamine stores and turnover in the subependymal layer and in the medial and lateral palisade zone of the median eminence. It is suggested that rGH may inhibit its own secretion partly via reduction of DA synthesis and release in the median eminence leading to increased somatostatin release and partly via reduced noradrenaline synthesis and turnover in the median eminence leading to reduced secretion of a growth hormone releasing factor.
The effects of acute audiogenic stress, with or without simultaneous nicotine treatment (0.3 mg/kg i.v.), on catecholamine levels in discrete dopamine and noradrenaline nerve terminal systems of the hypothalamus, and on the secretion of adenohypophyseal hormones and of corticosterone, were studied using quantitative microfluorometric evaluations of catecholamine stores and radioimmunoassays for the determination of serum hormone levels. Audiogenic stress and nicotine induced very rapid and discrete decreases in noradrenaline levels in the subependymal layer (SEL), in the parvocellular part of nuc. paraventricularis hypothalamic (PA FP) and in the posterior periventricular hypothalamic systems, (PV II); the decreases were apparent 2 min following the onset of treatment. Increases of arterial blood pressure were observed after nicotine treatment but could not have been a major factor in producing the changes in catecholamine levels. These changes in NA levels may be related to the nicotine- and stress-induced increases of ACTH (SEL and PA FP) and prolactin secretion (PV II) found in the present experiments. Stress enhanced the rapid but variable increase in vasopressin secretion induced by nicotine, suggesting one possible mechanism by which stress combined with smoking can contribute to the development of increased arterial blood pressure and finally to sustained hypertension.
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A four week sino-aortic denervation produces an increase of adrenaline (A) turnover in the anterior but not the posterior hypothalamus and a selective reduction of dopamine stores in the anterior hypothalamus. Furthermore, the mean arterial blood pressure and heart rate are unchanged in conscious animals, and a selective increase in LH secretion is observed. The activation of a compensatory vasodepressor adrenergic mechanism in the anterior hypothalamus may in part be responsible for the maintenance of a normal mean arterial blood pressure after chronic sino-aortic denervation. The neurochemical changes in the hypothalamic area may also be related to the increase in LH secretion found after chronic sino-aortic denervation.
Human seminal plasma contains eight different prostaglandins belonging to the F series, i.e. PGF1 alpha, PGF2 alpha, 19-hydroxy-PGF1 alpha, 19-hydroxy PGF2 alpha, as well as the corresponding 8 beta-isomers. A systematic description of the mass spectrometric fragmentation of the 8 beta-isomers has not been previously reported. In the present study the prostaglandins were separated from human seminal plasma and analysed as methylester, trimethylsilylethers with gas chromatography mass spectrometry. All the eight F and 19-hydroxy F prostaglandins fragmented in the same manner, but the relative abundances of the formed ions varied in a typical way. Thus, the mass spectra of 8 beta-PGF1 alpha and 8 beta-19-hydroxy PGF1 alpha differed clearly from those of their 8 alpha-isomers, which could be used for identification and should be considered in selected ion monitoring. The ratio between the seminal plasma levels of 8 beta- and 8 alpha-isomers of 19-hydroxy F1 alpha was much higher than the corresponding ratio for the PGF1 alpha.
Estradurin (a polymer of 17-beta-oestradiol) has an inhibitory effect on the synthesis/secretion of PRL. This effect is assumed to be caused by the strong inhibitory effect of the drug on phosphatases. With increasing time of low doses of Estradurin (0.001 micrograms/ml) in vitro, the inhibitory effect on PRL secretion was overcome and the synthesis/secretion of PRL increased. The secretion of GH was unaffected in all concentrations (0.001-0.1 micrograms/ml) except 1 microgram/ml. A stimulatory effect of 17-beta-oestradiol (0.01 micrograms/ml) on the synthesis/secretion of PRL was suggested by the tissue from one post-pregnancy pituitary. Short time organ cultures from prolactinomas or tumors with a concomitant secretion of GH and PRL show no changes of GH or PRL secretion following incubation with (0.001-0.1 micrograms/ml) of 17-beta-oestradiol. However, electron microscopy of 17-beta-oestradiol incubated specimens revealed an increased number of lysosomes and inclusion bodies in the cell cytoplasm. Incubation with testosterone (0.001-1 microgram/ml) cause inhibition of PRL synthesis/secretion in two of three prolactinomas. In GH secreting tumours testosterone did not effect PRL or GH secretion in vitro when compared with controls. The ultrastructural analysis of specimens in which a decrease of PRL synthesis/secretion had occurred showed myelin figures in the cell cytoplasm and accumulations of amorphous electron dense inclusion bodies.
Maternal serum and amniotic hormone levels have been investigated in two groups of women in pregnancy weeks 18-21. One group (B) was composed of women with high alpha-fetoprotein levels in serum without fetal abnormality, and a matched control group (A) with normal alpha-fetoprotein levels in serum. Amongst group B women were four pregnancy complications: two spontaneous abortions, one premature delivery, and one cesarean section due to fetal asphyxia. Group B women were significantly different from group A women. Thus, higher maternal serum levels of total estriol (P = 0.030), testosterone (P = 0.016), and alpha-fetoprotein (P = 0.018) were noted in the presence of male fetuses; and higher hPL (P = 0.004), FSH (P = 0.037), and alpha-fetoprotein (P = 0.002) concentrations in women carrying female fetuses, who were accompanied by lower total estriol concentrations (P = 0.045). Differences between groups B and A in terms of amniotic fluid analyses were only related to female fetal sex. Thus, group B showed higher hPL (P = 0.028), testosterone (P = 0.020), and FSH (P = 0.006) levels, and lower alpha-fetoprotein (P = 0.013) concentrations. It is concluded that elevated maternal serum levels of alpha-fetoprotein are accompanied in female fetuses by an endocrine milieu different from that of matched controls. This difference may put the conceptus at a disadvantage, but the majority of the girls were born on time without signs of small-for-date.
Lesions in the periventricular hypothalamic area in male rats results in a "feminization" of steroid metabolizing enzymes in the liver. These lesions also resulted in a decrease of somatostatin levels in the median eminence. Since blockade of somatostatin by in vivo administration of an antiserum also caused "feminization" of the liver, it is possible that at least one hypothalmic factor responsible for "feminization" is related to somatostatin. Also extrahypothalmic areas seem to influence sexually differentiated functions in the liver. The neuroendocrine control of the "feminizing factor" secretion from the pituitary bears several resemblances to the central control of GH. The hypothesis that the plasma pattern of GH regulates hepatic steroid metabolism in the rat was studied in two different animal models: (1) Different plasma patterns of GH were achieved by administration of human GH (hGH) at different frequencies or by infusing the hormone continuously by means of Alzet osmotic minipumps to hypophysectomized female rats. (2) The plasma pattern of GH in animals with an intact pituitary gland was investigated under conditions which lead to "feminization" of hepatic steroid metabolism. The results demonstrate that the plasma pattern of GH influences hepatic steroid metabolism. Increased trough plasma GH values or absence of time periods with undetectable plasma levels of GH appears to be a major determinant for "feminization" of hepatic steroid metabolism. Since sex steroids were found to influence the plasma pattern of GH it seems as if differences in the plasma pattern of GH between male and female rats explain the sex-differentiated hepatic steroid metabolism.
Extraction with organic solvents of Tris-HCl buffer solutions containing microgram amounts of saturated 3-oxo-steroids, followed by evaporation of the organic solvent, produce a condensation product identified as the Tris-3-imino-derivative of the steroid. The yields range between 20-40%. The conditions governing the formation of the derivatives have been explored.
The present studies have shown that chronic antidepressant treatment with desipramine, imipramine, zimelidine and alaproclate led to adaptive changes in both pre- and postsynaptic 5-hydroxytryptamine (5-HT) receptor mechanisms which appear to result in 5-HT sub- or supersensitivity development depending upon the 5-HT nerve terminal systems analyzed. The results underline the heterogeneity of the central 5-HT neurone systems in their responses to chronic antidepressant treatment. An involvement of 5-HT comodulators is postulated in the actions of antidepressants on central 5-HT synapses. Finally, the results point to the importance of 5-HT neurone systems as targets for the action for antidepressant drugs and they may mediate at least some of the therapeutic activity of antidepressant drugs.
Subacute treatment with toluene leads to a dose-related reduction of affinity in the [3H]spiperone binding sites labeling striatal dopamine (DA) receptors of the D2 type and cortical [3H]5-hydroxytryptamine (5-HT)-binding sites. It is suggested that these results represent a down regulation of activity at striatal DA and cortical 5-HT synapses, since they now may operate at higher concentrations of transmitters. The reduced affinity may be caused by the physicochemical properties of toluene leading to changes in membrane fluidity and thus in the regulation of DA and 5-HT receptors in the local circuits of the striatum and the dorsal cerebral cortex.
Total urinary estrogens (TUE) in morning urine samples delivered during seven days around midcycle from 14 normally menstruating women were analyzed and the results were compared with those obtained by radioimmunoassay of serum estradiol-17 beta (E2) and LH. The Spinnbarkeit of the cervical mucus was also determined daily and ovulation was confirmed by RIA of serum progesterone. Significant correlations (p less than 0.01) between day of peak levels of serum E2 and the day with the highest TUE value were obtained. Peak values for Spinnbarkeit, estradiol, TUE and LH were on the average obtained on cycle day 13.1 (10-17), 13.3 (10-16), 13.9 (11-18) and 14.1 (11-17), respectively, and the mean cycle length was 27.9 (24-32) days. The difference in mean peak day for estradiol and TUE, estradiol and Spinnbarkeit, estradiol and LH was significant in each comparison (p less than 0.01). Assays of TUE in morning samples as compared to analysis of TUE in 24 h urine portions were compared during 48 h in 10 women. The day with the highest TUE excretion was found to be the same in 7 women irrespective of the type of urinary sample analyzed. Analysis of urinary creatinine did not improve the TUE results. Levels of TUE in normally cycling females (n = 14); in women taking contraceptive steroids (n = 10), in menopausal women (n = 10) and in normal men (n = 10) agreed with those previously reported. It is concluded that the TUE determination by RIA may be helpful as a rapid method for everyday clinical use.
Fifty unilaterally cryptorchid boys aged 3 to 8 years were randomly and blindly allocated to treatment with luteinizing hormone releasing hormone or placebo intranasally. In the treated group, no significant descent of the undescended testis was found, whereas a minor downward movement of the scrotal testis occurred (P less than 0.001), probably as a result of decreased retraction by the cremaster muscle. Basal serum testosterone concentrations and testicular volume increased after treatment (P less than 0.01 and P less than 0.001, respectively). The response to an acute LHRH test, 100 micrograms/m2 body surface IV, before and after treatment, showed an increase in the luteinizing hormone peak value and a decrease in the follicle-stimulating hormone response in a significant number of patients (P less than 0.001). In the individual patient, there was a positive correlation between the increase in basal serum testosterone concentration and the degree of downward movement of the undescended testis (P less than 0.05).
Psychoendocrine and metabolic effects of social isolation and understimulation in real life were examined in a controlled study of 60 elderly people representative of their age group. Together with the staff and the elderly, a social activation program was formed at a senior citizen apartment building. Half of the elderly were part of this activation program (experimental group). The other half constituted the control group. Blood sampling and psychosocial testing were performed immediately before and after 3 and 6 months of social activation. Social activation increased threefold in the experimental group. Height decreased in the control group compared to the experimental subjects. Plasma levels of testosterone, dehydroepiandrosterone, and estradiol increased significantly in the experimental group over the 6-month period compared to the control group. The most pronounced increase took place during the initial 3 months. Hemoglobin A1c decreased significantly in the experimental group over the 6-month period compared to the control group. In this preliminary study it is concluded that social isolation and understimulation may be associated with a wide range of psychophysiologic effects in elderly people.
Immobilization stress (1 h) induced discrete reductions in noradrenaline (NA) levels in the posterior periventricular hypothalamic region and in the paraventricular hypothalamic nucleus, and a decrease in dopamine (DA) turnover in the medial palisade zone (MPZ) of the median eminence, but failed to induce regional increases of hypothalamic NA turnover. Stress also stimulated the secretion of ACTH, corticosterone and prolactin, while vasopressin, LH and FSH serum levels were unaffected. The stress induced reduction of DA turnover in MPZ may mediate the stress induced increase of prolactin secretion. Nicotine (0.3 mg/kg, s.c., 1 h) did not by itself significantly influence catecholamine (CA) turnover in the various CA nerve terminal systems analyzed in the hypothalamus, but reduced NA levels in the subependymal layer (SEL) of the median eminence. Nicotine administration did not affect the serum levels of any of the hormones evaluated. Nicotine counteracted to a minor degree the immobilization stress-induced reduction in NA levels, and also the stress-induced secretion of ACTH, but not of prolactin suggesting the involvement of noradrenergic mechanisms possibly in the paraventricular nucleus in the nicotine modulation of stress induced increases of ACTH secretion. The nicotine-induced reduction of NA levels in SEL was blocked by stress as well as the tendency for nicotine induced increases of dopamine (DA) turnover in the medial and lateral palisade zones of the median eminence indicating opposing influences of immobilization stress and nicotine on at least some hypothalamic CA systems.
The present findings show that nicotine given i.v. can within minutes induce increases of ACTH, vasopressin and prolactin secretion in the male rat, giving further evidence for the existence of nicotine-like cholinergic receptors involved in the regulation of these hormones. These changes were associated with rapid reductions of NA levels in the subependymal layer of the median eminence, in the nuc, dorsomedialis hypothalami and in the anterior and posterior periventricular hypothalamic area as revealed by quantitative microfluorimetrical measurements of CA fluorescence. Intraindividual correlations indicate the involvement of an inhibitory noradrenergic mechanism in the subependymal layer of the median eminence in the regulation of ACTH secretion, the involvement of noradrenergic mechanisms in the posterior periventricular area in the regulation of prolactin secretion and the involvement of dopaminergic mechanisms in the medial palisade zone of the median eminence in the regulation of prolactin secretion. A rapid rise of prolactin secretion seems to be associated mainly with a reduction of NA levels in the posterior periventricular area indicating the existence of a possible facilitatory noradrenergic mechanism in this region regulating prolactin secretion.
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