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Biomedical subjects

R Demura

Publications and source records attributed to R Demura.

At least 109 records · Page 6Linked to original sources
PubMed1981

Plasma pituitary hormone responses to the synthetic enkephalin analog (FK 33-824) in normal subjects and patients with pituitary diseases.

D-Ala, Mephe, Met, enkephalin (Sandoz FK 33-824) is a stable long acting analog of methionine-enkephalin. FK 33-824 (0.5 or 1.0 mg), elicited plasma GH and PRL responses in normal subjects. In 23 patients with pituitary dwarfism, the response of plasma GH was markedly impaired, while PRL responded to a variable degree. In patients with acromegaly, there was little or no increase in GH and PRL after FK 33-824. Plasma GH increased to a variable degree after FK 33-824 in patients with hyperprolactinemia, with little change in plasma PRL. FK 33-824 decreased plasma cortisol in normal subjects and patients with pituitary disease. These results show that patients with acromegaly and hyperprolactinemia due to pituitary adenomas and patients with pituitary dwarfism do not respond well to FK 33-824, presumably because of hypothalamic or pituitary derangement.

Acromegaly↗
PubMed1981

[Laron's dwarfism].

Explore the source record for details and available documents.

Dwarfism, Pituitary↗
PubMed1980

Ultrastructure, immunohistochemistry and hormone release of pituitary adenomas in relation to prolactin production.

Fifteen cases of pituitary adenoma, 14 of which were associated with hyperprolactinemia, were studied by observation and granule morphometry of electron micrographs, immunohistochemistry and sequential observation of in vitro release with regard to hormone production, storage and secretion. Adenoma cells of 6 cases with marked elevation of plasma prolactin were sparsely granulated, showed characteristic ultrastructures including the presence of small secretory granules, well developed Golgi and rough membranes, misplaced exocytosis, and positive or negative immunostaining for prolactin. These adenomas also showed vigorous release of the hormone into the circulation and/or culture medium. In vitro studies showed that negative immunostaining of adenoma cells did not preclude the production and secretion of the hormone. One densely granulated adenoma containing cells with numerous lactotroph type granules showed moderate release of prolactin into the circulation. In an acromegalic case associated with both high plasma growth hormone and prolactin, some cells were shown by immunohistochemistry to store both hormones There were 4 adenomas which could not be shown to produce, store and secrete prolactin by any method available.

Adenoma↗
PubMed1980

Effects of chlorpromazine and naloxone on growth hormone secretion in rats.

The present study was conducted to examine roles of brain monoamines and opioid peptides in growth hormone (GH) secretion in unanesthetized, freely behaving rats. The administration of chlorpromazine (CPZ, 300 microgram/100 g, i.v.), an antagonist of brain monoamines, to rats that were passively immunized with antiserum to somatostatin immediately lowered plasma GH levels and inhibited episodic GH secretion. An intraventricular injection of beta-endorphin (3.5 microgram) stimulated GH secretion. This effect was completely inhibited by the prior administration of naloxone (100 microgram/100 g, i.v.), a specific antagonist of opioid peptides, but not by CPZ. In addition, the administration of naloxone did not inhibit episodic GH secretion. The results suggest that CPZ inhibits episodic GH secretion via a factor(s) other than somatostatin. It is also inferred that brain monoamines, but not opioid peptides, play major roles in the regulation of episodic GH secretion in rats.

Animals↗
PubMed1980

Failure of naloxone to influence plasma growth hormone, prolactin, and cortisol secretions induced by insulin hypoglycemia.

The effect of naloxone, a specific antagonist of opioid peptides, on plasma, GH, PRL, and cortisol responses to insulin-induced hypoglycemia was studied in five healthy male subjects. The iv administration of regular insulin (0.15 U/kg) led to similar degrees of hypoglycemia on control and experimental days. Plasma GH, PRL, and cortisol levels rose significantly in response to insulin-induced hypoglycemia. A 2-h infusion of naloxone (0.8 mg/h) started 30 min before insulin injection did not alter either basal hormone levels or the hormone responses to insulin-induced hypoglycemia. These results suggest that endogenous opioid peptides do not play a major role in GH, PRL, or cortisol secretion induced by insulin hypoglycemia.

Adult↗
PubMed1980

Anterior pituitary hormones in plasma and pituitaries from patients with Cushing's disease.

Pituitary adenomas were obtained from eight of nine patients with Cushing's disease, and the surrounding tissues as well were obtained from six of nine patients. ACTH, beta-lipotropin (beta-LPH), beta-endorphin, GH, TSH, LH, and PRL concentrations in these tissues were determined by RIA. Immunoreactive ACTH and beta-endorphin (beta-endorphin + beta-LPH) were present in high concentrations in all adenomas, and low concentrations were found in the surrounding tissues, except for one patient. As compared to levels seen in normal pituitary tissue, the GH concentration in the surrounding tissues was suppressed in five of six cases. TSH and LH concentrations were suppressed in four and three cases, respectively. The PRL concentration was not suppressed in any of the six patients studied. These four hormones were not detected in any adenoma. Plasma GH, TSH, and LH responses to various stimuli which were suppressed preoperatively returned to normal in most of the patients after adenomectomy. Basal plasma cortisol concentrations were normal or subnormal and were suppressed by the administration of 1 mg dexamethasone after adenomectomy, in contrast to the lack of such suppression preoperatively. ACTH and beta-endorphin secretion were stimulated by lysine-8-vasopressin and suppressed by dexamethasone and cyproheptadine in vitro.

Adenoma↗
PubMed1980

[Pituitary adrenocortical response to high dose administration of betamethasone in neurosurgical patients (author's transl)].

Using RIA technique, response patterns of ACTH-adrenocortical system to short term large dose corticosteroid therapy for neurosurgical patients were investigated. The subjects were consisted of 20 males and 13 females, ageing ranging from 10 to 60 years old. The subjects were divided into three groups according to mode of steroid administration. In the first group, 12 mg/day of betamethasone were administered for 5 days and cancelled without gradual reduction. In the second group, 12 mg/day of betamethasone were administered for 4 days and 6 mg/day of betamethasone were given for following 2 days. In the third group, 12 mg/day of betamethasone were administered for 3 days and gradual reduction of betamethasone was given for following 4-5 days. Response of plasma cortisol level to synthetic 18-ACTH were measured in all patients for 3 days after betamethasone administration cancelled. The results led to the following conclusion. 1) The second and third groups had not any clinical symptom after steroid cancelled, but one half cases of the first group had mild headache, nausea for 2 days after cancelled. 2) Recovery process of adrenocortical function in the second group is most rapidly, compared with that in other two groups. 3) In the postoperative steroid therapy in neurosurgery, it could be concluded that 4 days massive administration of steroid followed by stepwise reduction in 2 days would be functionally well tolerated by adrenocortical system.

Adolescent↗
PubMed1979

ACTH, beta-LPH and beta-endorphin in pituitary adenomas of the patients with Cushing's disease: activation of beta-LPH conversion to beta-endorphin.

ACTH, beta-lipotropin (beta-LPH) and beta-endorphin concentrations were determined in pituitary adenomas of the patients with Cushing's disease. Immunoreactive ACTH and beta-endorphin were present in high concentrations and essentially equimolar amounts in pituitary adenomas. beta-LPH conversion to beta-endorphin was activated in pituitaries associated with ACTH/beta-LPH producing adenomas. Immunoreactive ACTH and beta-endorphin concentrations were markedly suppressed in the surrounding tissues.

Adenoma↗
PubMed1979

A case of histiocytosis X associated with panhypopituitarism and hyperimmunoglobulinemia G and E.

A 43 year old man with diabetes insipidus who showed panhypopituitarism and marked hypergammaglobulinemia due to histiocytosis X is reported. His low basal plasma adrenocorticotropin (ACTH) and growth hormone (GH) failed to respond to insulin-induced hypoglycemia. His basal serum thyroid hormone level was below normal and normal basal plasma thyrotropin (TSH) showed a delayed response with normal peak value to TSH-releasing hormone (TRH). Normal basal plasma pituitary gonadotropin also showed a delayed response with normal peak value to luteinizing hormone-releasing hormone (LH-RH). Suppression of plasma prolactin (PRL) by levodopa (l-dopa) was impaired and elevation of basal plasma PRL was noted at the second admission. These results, combined with diabetes insipidus, suggested that the panhypopituitarism in these patients was hypothalamic in origin. The polyclonal hypergammaglobulinemia was characterized by elevated serum IgG and IgE levels which returned to normal after corticosteroid treatment with concomitant clinical improvement. Elevated serum IgE levels, tissue and peripheral eosinophilia, and the effectiveness of corticosteroid therapy support the hypothesis that some allergic mechanism may be involved in the pathogenesis of this disease.

Adrenocorticotropic Hormone↗
PubMed1979

Chlorpromazine inhibits episodic growth hormone secretion in the rat.

Effects of chlorpromazine (CPZ) on plasma GH and prolactin levels were observed in conscious rats provided with chronic indwelling right atrial cannulae. The administration of CPZ (200 micrograms/100 g b.w. iv) suppressed episodic plasma GH burst and resulted in significant elevations of plasma prolactin levels. These were also observed in rats in which two types of hypothalamic deafferentation, i.e. anterior and complete, had been carried out. The data suggest that CPZ acts within the medial basal hypothalamus and inhibits episodic plasma GH secretion. In addition, it is inferred that catecholamines are involved in the generation of episodic plasma GH burst.

Animals↗