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Biomedical subjects

H Hosogi

Publications and source records attributed to H Hosogi.

15 recordsLinked to original sources
PubMed1979

Specificity of cultured anterior pituitary cells in detecting corticotropin releasing factor(s): the effect of biologically active peptides and neurotransmitter substances on ACTH release in pituitary cell cultures.

Biologically active peptides and neurotransmitter substances were added to anterior pituitary cell cultures to examine the presence of corticotropin releasing factor (CRF)-like activity. Hypothalamic extract (HE) induced significant dose-related increase of ACTH, and the lowest effective dose was 0.01 HE/ml. Other tested substances including luteinizing hormone-releasing hormone, thyrotropin releasing hormone, melanocyte stimulating hormone release inhibiting factor, somatostatin, substance P, neurotensin, beta-endorphin. leu-enkephalin, met-enkephalin, bradykinin, norepinephrine, dopamine, serotonin, acetylcholine, histamine, gamma-amino butyric acid or gamma-hydroxy butyric acid showed no CRF-like activity. Relatively high doses of lysine vasopressin, arginine vasopressin and angiotensin II increased the release of ACTH in pituitary cell cultures, but the maximal ACTH response was markedly less than with HE. These results indicate that cultured anterior pituitary cells are sensitive and fairly specific in detecting CRF(s) comparing with other detecting procedures.

Adrenocorticotropic Hormone↗
PubMed1978

Effect of glucagon on growth hormone secretion in rats.

Gentled rats injected subcutaneously with glucagon (20 microgram/100 g body weight) showed a significant decrease in plasma growth hormone (GH) at 15 min after glucagon injection. A subcutaneous injection of 50% glucose did not cause the early suppression as shown at 15 min after glucagon injection, but at 30 min after glucose injection a tendency to decrease in plasma GH was observed. In urethane anesthetized rats, a subcutaneous administration of glucagon (1 microgram or 10 microgram/100 g body weight) failed to elicit an increase in plasma GH. In vitro incubation of anterior pituitary fragments with glucagon failed to decrease the release of GH, suggesting that glucagon does not act directly on the anterior pituitary.

Anesthesia, General↗
PubMed1978

[Measurement of rat serum corticosterone using radiostereoassay kit for cortisol (author's transl)].

A very simple technique for measurement of rat serum corticosterone with radiostereoassy kit using 75Se-cortisol was devised. Only 25--50 microliter serum was required for this assay. The serum sample was first diluted to 300 microliter with water and heated in a glass tube to denature the endogeneous cortisol binding protein. Then an aliquot of the sample was transferred into an assay vial containing 75Se-cortisol, cortisol binding protein and adsorbent granules. After rotated, an aliquot of the supernatant was taken for counting. High level of rat serum corticosterone was measured with satisfying accuracy by dilution with water. Serum corticosterone levels in 7 normal female Sprague-Dawley rats (7 weeks old, Ca 200g body weight) at 2.00 pm were 29.5 +/- 12.2 microgram/dl (mean +/- SD). The levels were lower and higher in rats treated with dexamethasone and with 1-18 ACTH, respectively.

Animals↗
PubMed1977

Transient appearance of a provocative growth hormone response to L-dopa following incomplete adenomectomy in an acromegalic patient.

A 33-year female patient with active acromegaly and hyperthyroidism was examined before and after incomplete removal of a pituitary adenoma. Before adenomectomy the mean basal plasma GH level was 786+/-189 ng/ml. After surgery this value decreased to 251+/-22 ng/ml. Before surgery L-dopa decreased the plasma GH levels, but after adenomectomy normal GH responses were transiently observed to L-dopa. At 10 months after incomplete surgery the GH response to L-dopa became abnormal again despite a lower GH concentration. These findings suggest that the abnormal GH response to L-dopa may be due to a short-loop negative feedback system which was reset by an elevated GH level.

Acromegaly↗
PubMed1976

[In vitro assay for ACTH-releasing activity using ACTH radioimmunoassay: ACTH releasing activities by various drugs (author's transl)].

Several procedures have been reported for the assay of corticotrophine-releasing factor (CRF), each having its advantages and disadvantages. This report deals with an in vitro assay of ACTH releasing activity utilizing pituitary incubation combined with ACTH radioimmunoassay. Rat half pituitary was preincubated in 2 ml Krebs Ringer bicarbonate buffer containing 0.2% glucose and 0.25 % BSA (KRBG-BSA) for 1.5 hr (45 min X 2). The medium was replaced by 1 ml KRBG-BSA and incubated for 30 min. Then the medium was again replaced by 1 ml KRBG-BSA or KRBG-BSA containing test materials and incubated for another 30 min. The amount of ACTH assayed by radioimmunoassay in the 2nd 30 min incubation was compared with in the 1st 30 min incubation and expressed as percentage. In ACTH radioimmunoassay, anti-ACTH serum was diluted to 1 : 1,500-3,000. The 125I-alpha 1-24ACTH-antibody system was not affected by lysine-vasopressin (LVP), arginine-vasopressin (AVP), rat's pituitary LH, GH and prolactin. Human 1-39ACTH was used as ACTH standard, and the dilution curve of incubation medium was paralleled with the standard curve. Repeatability of immunoassayable ACTH within-assay was 174 +/- 5.0 pg/tube (CV = 2.9%). A log dose-relationship was observed between the amounts of stalk median eminence extracts (SME ; NIAMDD) added to the incubation medium and its ACTH releasing activities. The sensitivity of this assay method was at least 0.1 SME or 10 mU of LVP and AVP. Using this method, it found that LVP, AVP, norepinephrine (100 ng/ml200 ng/ml) and 5-hydroxytryptophane (1 mug/ml) had ACTH releasing activities but LH-RH, TRH, glucagon, dopamine, phentolamine, propranolol, haloperidol, prostaglandin E1 and indomethacin did not affect the release of ACTH.

5-Hydroxytryptophan↗
PubMed1976

[Hypothalamic-hypophyseal-adrenocortical dysfunction in patients with anorexia nervosa (author's transl)].

Hypothalamic-pituitary-adrenocortical function was investigated in 14 patients with anorexia nervosa. Impaired suppression of plasma cortisol by dexamethasone was revealed. In 14 patients with anorexia nervosa, circadian rhythm of plasma cortisol, insulin tolerance test, rapid ACTH test and overnight dexamethasone suppression test were examined. Levels of plasma cortisol were higher than those in control subjects throughout the day, and normal circadian rhythm of plasma cortisol was not observed. Basal levels of plasma ACTH were within normal range. tthe response of plasma cortisol to insulin-induced hypoglycemia was lower than that in control subjects, while the response of plasma cortisol in rapid Acth test was normal. In overnight suppression tests, in which one mg dexamethasone was administered orally, 11 of 14 patients showed no suppression of plasma cortisol and 3 other patients showed incomplete suppression. Elevated levels of plasma cortisol and the absence of normal circadian rhythm in patients with anorexia nervosa and malnutrition have already been reported by other investigators, and these abnormalities were ascribed to the delayed half life of plasma cortisol due to impaired cortisol metabolism. However, according to our investigation, it is difficult to explain the failure of dexamethasone to suppress cortisol only by the delayed half life of plasma cortisol, and it is supposed that some kind of abnormal hypothalamic control is also involved.

17-Ketosteroids↗
PubMed1976

Plasma immunoassayable ACTH levels during and after hydrocortisone infusion in patients with Cushing's disease.

The plasma ACTH responses to hydrocortisone infusion were compared in patients with Cushing's disease and primary adrenocortical insufficiency. In 4 patients with primary adrenocortical insufficiency, plasma ACTH levels were suppressed exponentially after administration of a relatively large dose of hydrocortisone (1.0 mg/kg/1.5 hr-3.0 mg/kg/2 hr). In patients with post-adrenalectomized Cushing's disease (4, bilateral; 1, unilateral), plasma ACTH suppression was delayed. Plasma ACTH levels, expressed as a percentage of the basal concentrations, were significantly less suppressed in patients with Cushing's disease than in patients with primary adrenocortical insufficiency 90 (p less than 0.05) and 120 (p less than 0.05) min after the beginning of infusion. When 0.5 mg/kg hydrocortisone was infused over a period of 1.5 hr, suppression was also delayed in Cushing's disease, and plasma ACTH levels were less suppressed in 4 patients with Cushing's disease than in 4 patients with primary adrenocortical insufficiency at 30 (p greater than 0.05), 45 (p greater than 0.05) 60 (p less than 0.05) min.

Adolescent↗
PubMed1976

Hypothalamic pituitary adrenal function in patients with anorexia nervosa.

Hypothalamic pituitary adrenal function was studied in 14 patients with anorexia nervosa. Although basal plasma cortisol levels in the morning were elevated in most cases, basal plasma ACTH levels were not suppressed. Oral administration of 1 mg dexamethasone 10 hr before blood sampling failed to suppress plasma ACTH and cortisol levels in most patients with anorexia nervosa. Apparent biological half-life of exogenous cortisol was prolonged in all 4 patients with anorexia nervosa tested. The cortisol response to insulin-induced hypoglycemia and exogenous ACTH appeared to be blunted in these patients. It is concluded that anorexia nervosa has dysfunctions of hypothalamic pituitary adrenal axis, especially an abnormal feedback mechanism on ACTH secretion.

Adolescent↗
PubMed1975

[Comparison with growth hormone responses to various drugs or substances in patients with active acromegaly (author's transl)].

Growth hormone (GH) responses to L-dopa, 2-Br-alpha-ergocryptine (CB-154), thyrotropine-releasing hormone (TRH), luteinizing hormone-releasing hormone (LH-RH), glucagon and glucose were investigated in six patients with active acromegaly. The following results were obtained. 1) Subcutaneous injection of 1 mg glucagon caused a clear-cut decrease in plasma GH levels in 5 out of 6 active acromegalic patients at 30 minutes after the injection. In 2 out of 6 patients a rebound of plasma GH was observed. 2) In three out of six patients with active acromegaly, oral administration of 0.5 g L-dopa caused a significant suppression of plasma GH levels. 3) CB-154 (2.5mg) administered orally elicited a marked decrease in plasma GH levels in the same three patients who showed a significant suppressive GH reponse to L-dopa, and the inhibitory effect of CB-154 on GH secretion lasted for 6 hours. These patients who had a GH response to L-dopa or CB-154 were named "responders". 4) Intravenous administration of TRH resulted in a significant increase in plasma GH in 4 patients 3 of whom were responders and the other a non-responder. 5) Pretreatment with CB-154 did not modify the TRH-induced GH increase in all patients who had a positive response to TRH. 6) A significant increase in plasma GH was elicited by the intravenous injection of 100 mug LH-RH in 3 out of 6 patients with acromegaly. 7) When oral administration of CB-154 had been given 2 hours before LH-RH, the GH response to LH-RH was blunted in two of three patients who had a LH-RH-induced increase in plasma GH levels.

Acromegaly↗
PubMed1975

[Solid phase radioimmunoassay for plasma testosterone using plastic microtiter tray (author's transl)].

UNLABELLED: In order to simply radioimmunoassay for plasma testosterone and to measure many samples at the same time, a method of solid phase radioimmunoassay utilizing a plastic disposable microtiter tray (DMT) by which chromatography can be omitted was investigated. METHOD: The antiserum was obtained by immunizing rabbits with testosterone-3 BSA which had been synthesized according to the Erlarnger's method. Plasma samples (male: 0.05ml, female: 0.2 ml) were extracted with 1.0 ml of ether. After freezing the plasma layer in an acetone-dryice bath, the ether phase was transfered to a glass tube and evaporated to dryness. These samples and the dried standard testosterone were dissolved with borate buffer containing 3H-testosterone and transfered to plastic DMT which had been precoated with the diluted antiserum, and incubated for 24 hrs. After removal of the incubated solution, the cups of DMT were cut off and were dissolved with toluene scintillator in counting vials. The radioactivity was counted with a liquid scintillation counter. RESULT: Other steroids except for 5alpha-dihydrotestosterone (5alpha-DHT) had a low degree of cross reactivity with the antiserum. Five alpha-DHT which could be measured together with testosterone in this assay was not a problem clinically because of its strong androgenic activity. The best standard curve was obtained when the antiserum was diluted to 1:1000. The sensitivity of this assay was 10 pg/tube. The maximal adsorption of antibody to plastic DMT was observed when the pH of antiserum was within the range of 6.5-9.5 and the precoating time was 24 hr at room termperature. The best pH of incubation buffer was 8.0, and the antigen-antibody reaction became a plateau when the incubation exceeded 6 hrs. Water blank in this assay was 4.6 +/- 2.1 pg/tube. The recovery of testosterone (50, 100, 200 pg) added to 0.1 ml female plasma was 99 +/- 6.8%. Coefficients of variation within assay and between assay were below 11.2% and 20.0%, respectively. Correlation between this method and the dextran-coated charcoal method was fairly good (r=0.938). Plasma testosterone levels in 10 normal males and 12 normal females were 616 +/- 202 (mean +/- SD) ng/dl and 66 +/- 29 (mean +/- SD) ng/dl, respectively. The levels were low in patients with hypopituitarism, hypogonadism and acromegaly. They were normal in patients with Cushing's syndrome due to adrenal hyperplasia and adenoma, but they were high in a patient with adrenal carcinoma. In a patient with testicular feminization, the level was 632 ng/dl. This increased after the administration of HCG, and decreased to 127.5 ng/dl after castration. This solid phase radioimmunoassay (using plastic DMT) is economically feasible as well as simple because it is possible to separate the bound hormone from the free hormone of all samples at the same time and there is little restriction in time and temperature. According to the above results, this method is suitable for routine clinical use.

Acromegaly↗
PubMed1975

Suppression of serum growth hormone levels by glucagon in patients with active acromegaly.

One mg of glucagon was given subcutaneously to eight patients with active acromegaly. Seven out of eight patients had a rapid decrease in serum growth hormone (GH) levels at 30 min after the glucagon injection. In two out of seven patients a rebound increase in serum GH following the early GH reduction was observed. On the other hand, oral administration of 50 g glucose which caused a comparable increase in blood glucose to that after the glucagon injection elicited no early suppression in serum GH levels in the same patients. These data suggest that the inhibition of GH release induced by glucagon could not be related to the increase in blood glucose by glucagon.

Acromegaly↗