Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 8 patients with diabetic ketoacidosis, serum prolactin was measured and found to be elevated (24.8 +/- 10.2 ng/ml, mean +/- SEM). After correction of the ketoacidosis, the prolactin level decreased to 10.9 +/- 6.4 ng/ml (normal range men 4.9 +/-0.8, women 5.1 +/- 1.6 ng/ml). The scatter of prolactin values was wide. A study of the correlation between the serum prolactin values and chemical parameters that are altered in diabetic ketoacidosis was therefore undertaken. Serum prolactin values did not correlate well with the serum bicarbonate concentration or serum osmolality. However, a significant negative correlation between log serum prolactin concentration and serum sodium concentration was demonstrated (r = -0.61, P less than 0.01). It is suggested that serum prolactin may possible participate in sodium retention in man as has been demonstrated in studies on animals.
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PMID:Increased serum prolactin in diabetic ketoacidosis; correlation between serum sodium and serum prolacting concentration. 1 57

Moderate hyperprolactinemia was found in 14 of 30 infertile patients with short luteal phase indicating a possible hypothalamic disorder in these patients. While the cycle length was normal, 28 days, late ovulation around day 18 of the cycle was characteristic of these patients. During bromocriptine treatment, 2.5 mg twice daily, ovulation took place earlier and luteal phase became longer irrespective of the basal serum prolactin level. The mean (+/- SEM) duration of luteal phase was 9.9 +/- 0.2 days in control cycles, and 11.7 +/- 0.5 and 12.2 +/- 0.3 days in two successive bromocriptine cycles (P less than 0.001). In patients taking bromocriptine, luteal phase became longer than 11 days in 37 of 60 treatment cycles, but no significant difference was recorded in the circulating progesterone and LH levels during mid- and late luteal phase. Three patients became pregnant and they all had normal baseline serum prolactin concentrations. Our results show that bromocriptine may be effective even when no apparent indication for prolactin suppression can be demonstrated.
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PMID:Prolactin levels and bromocriptine treatment of short luteal phase. 3 81

Seminal (i prolactin) immunoreactive prolactin was studied in 14 healthy subjects, ages 31 + or - 2 SEM, before and after undergoing elective vasectomy for birth control. Seminal plasma was separated within 2 hours of ejaculation, and prolactin was measured in duplicate by radioimmunoassay. The difference between the prevasectomy (mean + or - SEM 11.1 + or - 0.8 ng/ml) and postvasectomy seminal i prolactin (mean + or - SEM 9.9 + or - 0.7 ng/ml) was statistically significant (mean + or - SEM 1.21 + or - 0.53 ng/ml, paired t-test, t=2.36, P 0.05). The mean prevasectomy seminal prolactin correlated with the corresponding mean postvasectomy value of the same subject (linear regression analyses, r=0.77, P 0.001). This study suggested that the accessory sex organs were the major source of seminal immunoreactive prolactin, and that a minor contribution might come from the in vivo presence of spermatozoa and/or testicular secretions. It also suggested that the magnitude of seminal immunoreactive prolactin was characteristic for each individual.
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PMID:Inherent ranges of seminal prolactin in pre- and postvasectomy subjects. 4 2

Intravenous metoclopramide (MET) (10 mg) induced a brisk PRL response with a mean +/- SEM peak of 85.3 +/- 7.7 ng/ml maximal at 30 min. L-Dopa, but not atropine pre-treatment, attenuated the prolactin (PRL) response to MET. This indicates that the antidopaminergic properties of MET mediate PRL secretion. MET did not influence basal levels of TSH, LH or FSH. Neither did it affect their response to the respective releasing of hormones. Our results indicate that dopaminergic blockade induced by iv MET, does not influence the secretion of the pituitary glycoprotein hormones.
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PMID:Failure of metoclopramide to influence LH, FSH and TSH secretion or their responses to releasing hormones. 11 96

Somatomedin-like activity was measured in the plasma of growing lambs using the porcine costal cartilage disk assay. Plasma concentrations were found to be high initially at 2 days of age (mean potency 1.02 plus or minus 0.13 (SEM) units/ml, n = 4) declined significantly by 8 days of age (mean potency 0.65 plus or minus 0.04 units/ml, n = 5, P less than 0.01, analysis of variance). Thereafter somatomedin-like activity declined slowly to reach its lowest concentration at 146 days of age (mean potency 0.61 plus or minus 0.04 units/ml, n = 5) then it rose slowly until 288 days of age (mean potency 0.61 +/- 0.04 units/ml, n = 5. These changes in somatomedin-like activity were accompanied by high initial plasma concentrations of growth hormone (24.8 plus or minus 4.8 ng/ml, n = 5) which declined under 188 days of age (2.8 plus or minus 0.04 ng/ml, n- 5) and then rose slightly until 288 days of age (13.8 plus or minus 9 ng/ml, n=5). Plasma prolactin concentrations showed a different pattern being low initially (47.8 plus or minus 8.7 ng/ml, n = 5) rising until 146 days of age (203 plus or minus 16 ng/ml, n = 5) and then declining to low value for the rest of the experiment. The relationships between these factors is not clear but somatomedin-like activity shows a pattern in the lamb which is highest when growth is faster (i.e. in the young lamb).
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PMID:Changes in somatomedin-like activity and concentrations of growth hormone and prolactin in the plasma of castrated growing lambs. 26 80

The effect of a-adrenergic and dopaminergic blockade on the ability of pituitary-hypothalamic axis to produce an LH surge in response to oestrogen, was studied in eleven women treated with the neuroleptic agents haloperidol, fluphenazine or chlorpromazine. Seven women on no medication were controls. 6.6 mg of oestradiol benzoate (OB) was injected i.m. after control serum was obtained and daily serum samples were obtained for four additional days. Sera were assayed for total oestrogens, LH, FSH and prolactin. Six of seven women in the control group and eight of eleven women treated with neuroleptic agents had LH surges to OB challenge. The mean prolactin of the treated women was 33.1 +/- 3.6(SEM) ng/ml and the mean prolactin of the controls was 14.9 +/- 1.5(SEM) ng/ml, P less than 0.005). Elevated levels of circulating prolactin did not prevent an LH surge to OB challenge. These results indicate that even in subjects with catecholamine blockade, an LH surge can be induced. This contrasts to results obtained in rats and suggests that the control mechanism of LH surge production differs in rodents and humans.
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PMID:Positive feedback of oestrogen on LH secretion in women in neuroleptic drugs. 33 7

Thirty acromegalic subjects underwent chronic CB154 therapy (10-20 mg daily) for periods ranging from 3 months up to 2 years. In 18 out of 21 patients, who exhibited consistent HGH reduction following acute administration of the drug, there was also during chronic treatment, a suppression of the plasma HGH levels exceeding 50% of base line values, e.g. from mean daily values between 14-197 ng/ml (mean +/- SEM = 57.8 +/- 12.4 ng/ml pre-treatment) to 2-19 ng/ml (mean 8.3 +/- 1.2 ng/ml post-treatment). In 12 of the subjects who responsed to chronic CB154 treatment, the mean daily values of HGH were below 10 ng/ml. The suppression of plasma HGH was maintained unaltered throughout the whole course of therapy. In the 9 subjects, in whom no consistent HGH decrease was evidenced with acute CB154 administration, there was accordingly a minor or no suppression of HGH values during the chronic treatment. In 13 subjects, irrespective of the degree of their GH responses, the plasma prolactin levels were constantly inhibited by CB154; instead the drug failed to modify significantly the TRH or insulin-induced GH release. These changes in the hormonal parameters were paralleled by marked clinical amelioration and improvement of some of the metabolic alterations frequently encountered in acromegaly, e.g. reduced carbohydrate tolerance, increased insulin resistance, diminished fall of plasma phosphorus after insulin, decreased urinary excretion of phosphate, hyper-hydroxyprolinuria and hyper-calciuria. Collectively, these data demonstrate that CB154 thrapy is effective in reducing HGH hyper-secretion in many acromegalic patients during long-term treatment.
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PMID:Long-term treatment with 2-Br-alpha-ergocryptine in acromegaly. 40 32

The effect of estradiol and/or testosterone upon secretion by seminal vesicle in castrated and intact rats was assessed in young adult Sprague-Dawley rats, using light microscopy (LM), transmission (TEM) and scanning (SEM)electron microscopy. Hormones were injected daily for ten days beginning ten days after castrations were performed. The normal rat seminal vesicle, as revealed by SEM, was characterized by a large saccular lumen with highly folded walls. Cell surfaces were covered with microvilli, or occasionally displayed a protruding, ruffled surface, sparsely covered with short microvilli. Cytology was normal in testosterone-treated animals. Estradiol treatment of castrated animals stimulated secretion by seminal vesicle epithelial cells as evidenced by the presence of normal secretory bodies, the presence of RER, and moderately hypertrophied Golgi complexes. These glands were not heavier than were glands from castrated, untreated animals, although the epithelial cells were significantly taller. Secretion was maintained in intact animals treated with estradiol, although glands were smaller and epithelial height was reduced. Estradiol and testosterone treatment in combination did not appear to have an additive effect on secretion, weight of the gland, or epithelial height. The following results support the hypothesis that estrogen-induced prolactin synthesis and release may be involved in the mechanism by which estradiol effected stimulation of seminal vesicle epithelium. Prolactin-treated, castrated animals exhibited focal areas of stimulated epithelium. In hypophysectomized animals (untreated controls), the seminal vesicle epithelium retained some secretory bodies and secretory fluid in the glandular lumen; epithelial height was taller than that in castrated controls. Estrogen treatment reduced the epithelial height to that of castrated controls; there was no evidence of secretion. This suggests that in the absence of anterior pituitary hormones, including prolactin, the stimulatory effect of estradiol on seminal vesicle epithelium was nullified. In adrenalectomized/castrated animals, estradiol treatment stimulated secretion in seminal vesicle epithelium just as in non-adrenalectomized/castrated animals. This indicates that the adrenal gland plays a non-essential role in the action of estrogen on seminal vesicle epithelium.
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PMID:Fine structural studies of rat seminal vesicle in castrated and intact animals following estrogen treatment. 43 95

In order to evaluate the possible role of prostaglandins in pituitary prolactin (PRL) secretion, PRL was serially measured following perphenazine (Trilafon) ingestion in 8 men before and after 5 days of indomethacin administration. Since estrogens have been shown to modulate prolactin secretion in man, serum steroids including estrone (E1), estradiol (E2), progesterone (P) and testosterone (T) were measured before and after indomethacin ingestion. Serum E1, P and T levels were similar during the pre- and post-indomethacin study periods: 56 +/- 4 (1 SEM) vs 48 +/- 5 pg/ml, 298 +/- 28 vs 315 +/- 32 pg/ml, and 8.1 +/- 0.7 vs 8.6 +/- 0.7 ng/ml, respectively. Serum E2 levels were slightly, but significantly, lower following indomethacin treatment at 30 +/- 3 vs 37 +/- 3 pg/ml (p less than .01). Basal serum PRL concentrations were unaffected by indomethacin administration (9 +/- 3 pre- vs 8 +/- 2 ng/ml post-drug treatment). Integrated perphenazine-induced PRL responses were likewise similar during the 2 study periods: 101 +/- 16 ng . hr/ml during the control period and 104 +/- 14 ng . hr/ml following indomethacin. Thus, short-term indomethacin treatment had no effect on basal or perphenazine-stimulated PRL secretion in men.
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PMID:Indomethacin fails to alter basal or phenothiazine-induced prolactin concentrations in man. 46 3

A sensitive and reproducible radioreceptor assay (RRA) for human growth hormone (HGH) is described. It allows the evaluation of HGH concentrations as low as 2 ng/ml. It has a limited cross-reactivity with human prolactin, which does not interfere at physiological levels in children. Comparison of the results with those of radioimmunoassay (RIA) showed no discrepancies in the serum of normal children before and after stimulation tests for GH (mean RRA/RIA ratio 1.03 +/- SEM 0.04, range 0.75 to 1.65) nor in the serum from hypopituitary dwarfs during the 12 h following an im injection of 6 mg of HGH (mean RRA/RIA ratio 1.05 +/- 0.04, range 0.84 to 1.28). It is concluded that receptoractivity of HGH is parallel to its immunoreactivity in normal children and in hypopituitary patients clinical grade HGH.
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PMID:Correlative study of radioreceptor assay and radioimmunoassay of serum growth hormone in children: normal children and HGH-treated pituitary dwarfs. 57 13


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