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Biomedical subjects

G M Besser

Publications and source records attributed to G M Besser.

At least 415 records · Page 23Linked to original sources
PubMed1979

Pregnancy in patients presenting with hyperprolactinaemia.

Ninety-two pregnancies occurred in 76 hyperprolactinaemic patients treated with bromocriptine. Half conceived within three months of attempted conception. There was no evidence of an increased rate of spontaneous abortion, fetal abnormality, or multiple pregnancy; the three twin pregnancies occurred in women who were additionally treated with clomiphene and human chorionic gonadotrophin. Thirty-one patients had radiological evidence of a pituitary tumour; 14 with major radiograph changes in the pituitary fossa or serum prolactin concentrations greater than 100 ng/ml received pituitary irradiation before conception. None of the latter showed evidence of enlargement of the tumour during pregnancy. In contrast two of the four patients with similar tumours but who were not irradiated developed visual field defects, one with gross destruction of the pituitary fossa. Prophylactic treatment to limit subsequent tumour expansion during pregnancy in patients with prolactinomas is indicated, and pituitary irradiation before conception appears to be a safe and effective method to achieve this goal.

Bromocriptine↗
PubMed1979

Acupuncture in heroin addicts; changes in Met-enkephalin and beta-endorphin in blood and cerebrospinal fluid.

In heroin addicts showing features of heroin withdrawal basal beta-endorphin levels were elevated in both blood and cerebrospinal fluid (CSF) and did not change during electroacupuncture, although this therapy suppressed the clinical features of withdrawal. Met-enkephalin levels were not elevated in blood or CSF before treatment. However, successful electroacupuncture was associated with a rise in CSF met-enkephalin levels in all patients studied, although concentrations in blood did not alter.

Acupuncture Therapy↗
PubMed1979

Reduction of pituitary-tumour size in patients with prolactinomas and acromegaly treated with bromocriptine with or without radiotherapy.

69 patients with prolactin-secreting or growth-hormone-secreting pituitary tumours were treated with bromocriptine with or without pituitary irradiation and followed up for 6 months to 6 1/2 years. Of 26 patients with prolactinomas, 11 had external pituitary irradiation in addition to bromocriptine. There was evidence of shrinkage of the pituitary tumour (either a reduction in fossa size or loss of visual-field defects) in 6 of these patients (23%), 3 of whom had been treated with bromocriptine alone. Of 43 acromegalic patients, 30 received external pituitary irradiation. 8 (19%) showed evidence of shrinkage of the pituitary tumour, including 2 who had received no radiotherapy. 1 patient treated with bromocriptine alone showed striking reduction in the size of his suprasellar extension, as assessed by serial computed-tomography scans over 11 months. At the same time his visual-field defects resolved and his deficient corticotrophin and thyrotrophin reserves returned to normal. Bromocriptine can reduce the size of both prolactin-secreting and growth-hormone-secreting pituitary tumours, and this is of potential importance in their management.

Acromegaly↗
PubMed1979

The effects of dopamine, bromocriptine, lergotrile and metoclopramide on prolactin release from continuously perfused columns of isolated rat pituitary cells.

The control of secretion of prolactin was studied using continuous perfusion of a column of isolated rat pituitary cells supported by Bio-Gel polyacrylamide beads. Prolactin secretion was inhibited repeatedly by dopamine and rapidly recovered in its absence. Maximum inhibition was achieved at 5 x 10(-7) M dopamine. Bromocriptine and lergotrile directly inhibited prolactin release from the pituitary cells. Bromocriptine had a longterm action in inhibiting secretion. The dopamine receptor blocking agent, metoclopramide, overcame the inhibitory effect of dopamine but had no effect on prolactin secretion in its absence.

Animals↗
PubMed1979

Comparison of long-acting analogues of luteinizing hormone releasing hormone in man.

Currently, LHRH, when used therapeutically, is given by parenteral injection every 8 h. We have looked at the release of LH and FSH induced by five analogues of LHRH and compared this with gonadotrophin release after synthetic LHRH. The analogues were substituted in position 6 or in positions 6 and 10 and were given intravenously, intranasally or subcutaneously in three separate studies. After intravenous administration of 100 micrograms, all analogues caused greater release of LH and FSH than did synthetic LHRH. Given intranasally in a dose of 500 micrograms, three of the four analogues tested caused greater LH and FSH release than did LHRH. With tryptophan substitution in position 6 (D-TRP6-LHRH), mean LH levels in five subjects were still above the normal range 24 h after a single intranasal dose. The intranasal administration of selected analogues of LHRH has great potential in the treatment of conditions associated with deficient gonadotrophin secretion, provided that pituitary overstimulation, which may eventually lead to a decrease in LH and FSH output by the anterior pituitary, is avoided.

Administration, Intranasal↗
PubMed1979

Effect of somatostatin on abnormal growth hormone and prolactin secretion in patients with the carcinoid syndrome.

Growth hormone (GH) secretion has been studied in two patients with the carcinoid syndrome during glucose loading and growth hormone-release inhibiting hormone (GHRIH, somatostatin) infusion. Both patients had elevated fasting GH levels which were not suppressed by glucose; GH levels fell rapidly during GHRIH infusion. One patient also had hyperprolactinaemia with galactorrhoea and the prolactin (PRL) levels were unaltered by GHRIH. The association between carcinoid tumours and abnormalities of GH and PRL secretion is discussed.

Adult↗
PubMed1979

Free-running circadian plasma cortisol rhythm in a blind human subject.

The plasma cortisol rhythm in man has been presumed to be an endogenous circadian rhythm, synchronized by some external stimulus to an exact 24-h period. Sleep/wake and 'social activity' cycles have been considered as candidates for this synchronizer. Previous studies have suggested that the dark/light phase shifts associated with the sleep-wake cycle may be the external synchronizer, rather than the sleep/wake cycle itself. A totally blind, but otherwise normal subject was studied for a period of 50 days. Her hourly sleep/wake status and hourly integrated mean plasma cortisol concentrations were determined, and the data were subjected to non-parametric mathematical analysis. The subject was found to have a free-running rhythm in plasma cortisol with a period of approximately 24.5 h. Her sleep/wake rhythm, determined by similar analysis, had a period of exactly 24 h. In addition to the dominant 24.5-h cortisol rhythm, there appeared to be a minor 24-h cortisol rhythm with a peak that coincided approximately with the time of awakening. It was not possible to determine whether this sleep/wake-related peak represented a minor component of the circadian rhythm, synchronized by some stimulus associated with sleep/wake activity, or merely an acute response to awakening itself. Nevertheless, the two rhythms exhibited 'beating' behaviour, resulting in maximal peak cortisol concentrations when they were in synchrony and minimal peak concentrations when they were not. It is concluded that environment dark/light phase shifts are the dominant synchronizer of the circadian rhythm in plasma cortisol concentrations in man, as they are for a variety of circadian rhythms in other living things.

Blindness↗
PubMed1979

The effect of lisuride hydrogen maleate, an ergot derivative on anterior pituitary hormone secretion in man.

The effects of single oral doses of 0.2 mg of lisuride hydrogen maleate, a semisynthetic ergot derivative, on serum levels of prolactin (PRL), growth hormone (GH), thyroid stimulating hormone (TSH), luteinizing hormone (LH), follicle stimulating hormone (FSH), cortisol and blood glucose were studied in six normal males. Lisuride effectively inhibited basal PRL secretion as well as the PRL response to TRH given 3 h later. In addition, the drug raised basal GH levels and decreased basal and TRH stimulated TSH secretion. No significant differences between lisuride and control were observed in basal LH and FSH, LHRH stimulated gonadotrophins or in cortisol. Drowsiness was noted by all subjects, one became nauseated and another vomited, 60 and 90 min respectively after administration of lisuride. No changes were seen in pulse rate and blood pressure. The endocrine effects of lisuride were attenuated by the prior administration of the dopamine antagonist metoclopramide. These results suggest that lisuride acts as a long-acting dopamine agonist and that therefore this drug could be of therapeutic use in hyperprolactinaemic states and acromegaly.

Adult↗
PubMed1979

Effects of the H2 receptor antagonist cimetidine on pituitary hormones in man.

The effects of the histamine (H2) receptor antagonist cimetidine on serum levels of prolactin (PRL), growth hormone (GH), thyroid stimulating hormone (TSH), luteinizing hormone (LH), follicle stimulating hormone (FSH) and cortisol were studied in five normal males. Cimetidine, when given by infusion at the dose of 100 mg/h for 5 h, did not alter adenohypophyseal secretion either basally or after pituitary stimulation with LHRH and TRH. However, 400 mg cimetidine given intravenously as a bolus injection significantly stimulated PRL release in all subjects, without affecting any other measured hormone. A dose-reponse relationship existed, and 200 mg cimetidine seems to be the minimum PRL-releasing dose when given as an intravenous bolus injection. These results suggest that cimetidine releases PRL and that this effect is dose-related, but only when large intravenous injections are given.

Adult↗
PubMed1979

Development and validation of a specific radioimmunoassay for somatostatin in human plasma.

Little is known about the factors controlling somatostatin secretion in man, and data are not available on the changes in circulating levels in various human physiological or pathophysiological states. This is mainly a consequence of the technical difficulties involved in measuring somatostatin in plasma. In the presence of plasma, binding of somatostatin tracer to antibody was consistently decreased by about 20%, and this could not be abolished by the addition of EDTA and aprotinin or by the use of specially prepared somatostatin-free plasma. Furthermore, in the presence of plasma, endogenous somatostatin does not dilute in parallel with synthetic cyclic somatostatin standard. We have, therefore, developed and validated a radioimmunoassay for somatostatin using prior extraction of the peptide onto leached silica glass. Tyrosine-II somatostatin was iodinated using lactoperoxidase and purified on ODS silica. This method is superior to iodination using chloramine-T with CMC cellulose purification, and gives a highly purified preparation with a shelf-life of at least eight weeks. Using this tracer and a specific antiserum, the limit of sensitivity of the assay was 10 pg/ml, with an intra-assay coefficient of variation of 12% (n = 16) and inter-assay coefficient of variation of 15% (n - 10). Parallelism has been demonstrated between standard synthetic cyclic somatostatin and all extracted plasma samples. The mean recovery of exogenous somatostatin from plasma was 78%. The fasting level of immunoreactive somatostatin at 0,900 hours in 40 normal subjects ranged from 17 to 81 pg/ml. Care is needed, however, when comparing these values with those obtained from other laboratories since standard preparations of somatostatin vary considerably in their immunopotency.

Antibody Specificity↗