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Biomedical subjects

K Chihara

Publications and source records attributed to K Chihara.

At least 397 records · Page 22Linked to original sources
PubMed1976

Plasma prolactin responses to thyrotropin-releasing hormone in patients with breast cancer.

Plasma human prolactin levels were measured by homologous radioimmunoassay in patients with primary breast cancer and in normal women of similar age. In normal controls mean (+/- SEM) basal plasma prolactin levels were 11.9 +/- 1.5 ng/ml and intravenous injection of synthetic thyrotropin-releasing hormone (TRH), 500 mug, caused a significant rise in plasma prolactin in all subjects examined with a maximum response of 52.6 +/- 3.3 ng/ml (mean +/- SEM). Markedly high plasma prolactin levels and exaggerated plasma prolactin responses to TRH were demonstrated in some patients with breast cancer. However, mean basal plasma prolactin levels and mean plasma prolactin increments following TRH in patients with breast cancer did not differ significantly from those in normal subjects. Plasma prolactin responses to TRH were slightly blunted during the administration of androgen in patients with breast cancer. These results suggest that some of the patients with primary breast cancer have abnormal prolactin secretion.

Adult↗
PubMed1976

Effect of sulpiride on plasma prolactin in rats.

I.v. injection of sulpiride (S; 0.5-20 mug/100 g b.w.) caused a significant and dose-related increase in plasma prolactin (Prl) levels in urethane-anesthetized rats, with peak values occuring 10 min after the injection. L-dopa administration (2 mg/100 g b.w., i.v.) significantly blunted plasma Prl response to S(1 mug/100 g b.w., i.v.). S injection (1 mug/rat) into a lateral ventricle also raised plasma Prl significantly. Hypothalamic destruction resulted in a prominent increase of basal plasma Prl, which increased further following the injection of S. These results suggest that S stimulates Prl secretion by its possible direct action on the anterior pituitary.

Animals↗
PubMed1976

Suppression by cyproheptadine of human growth hormone and cortisol secretion during sleep.

The effect of cyproheptadine on plasma growth hormone and cortisol levels was studied in seven male volunteers with polygraphic sleep monitoring. Sleep-related growth hormone release was completely inhibited in three of the seven normal subjects by the intravenous infusion of cyproheptadine (5 mg) which was started at the onset of sleep. In the other four, growth hormone release during sleep was significantly decreased or delayed by cyproheptadine when the drug infusion was started at 7:00 p.m., 1-2 h before the onset of sleep. The usual increase in plasma cortisol in the early morning was completely suppressed in all five subjects given cyproheptadine infusions from 4:00 to 7:00 a.m. The intravenous infusion of cyproheptadine increased slow wave sleep, although the time from sleep onset to the first occurrence of slow wave sleep was not affected. In contrast, rapid eye movement sleep was significantly decreased by cyproheptadine. These results suggest that cyproheptadine inhibits growth hormone and ACTH secretion during sleep in man, possibly by antagonizing serotoninergic mechanisms although other actions of the drug are not ruled out.

Adrenocorticotropic Hormone↗
PubMed1976

Stimulating and inhibiting effects of thyrotropin-releasing hormone on growth hormone release in rats.

The effect of thyrotropin-releasing hormone (TRH) on the mechanism regulating growth hormone (GH) secretion was investigated in urethane-anesthetized male rats. The iv injection of TRH (0.2 and 3 mug/100 g BW) caused a significant and dose-related increase in plasma GH. Greater GH responses to TRH were not obtained with doses of TRH larger than 5 mug/100 g BW. TRH injection also raised plasma GH in rats subjected to hypothalamic ablation, in which the maximum increments of plasma GH after TRH injection were greater than in control rats. Plasma GH responses to the iv injection of chlorpromazine (200 mug/100 g BW) were significantly augmented by the concomitant iv injection of TRH in a dose of 3 mug/100 g BW. However, a large dose of TRH (25 mug/100 g BW) injected with chlorpromazine caused a significantly smaller increase in plasma GH than did smaller doses of TRH (0.2 and 3 mug/100 g BW). TRH injection into the lateral ventricle (0.02 and 0.2 mug/100 g BW) inhibited significantly the GH release induced by chlorpromazine, whereas TRH (0.2 mug/100 g BW) alone caused only a slight increase in plasma GH. These results suggest that TRH may not only stimulate GH release by a direct action on the pituitary, but may also modify GH secretion by acting through the central nervous system.

Animals↗
PubMed1976

Effects of hyperthyroidism and hypothyroidism on rat growth hormone release induced by thyrotropin-releasing hormone.

The effect of synthetic thyrotropin-releasing hormone (TRH) on the release of growth hormone (GH) and thyroid-stimulating hormone (TSH) was investigated in euthyroid, hypothyroid, and hyperthyroid rats under urethane anesthesia. In euthyroid control rats, intravenous injection of TRH (200 ng/100 g BW) resulted in a significant increase in both plasma GH and TSH. In rats made hypothyroid by treatment with propylthiouracil or by thyroidectomy, basal GH and TSH levels were significantly elevated with exaggerated responses to TRH. In contrast, plasma GH and TSH responses to TRH were both significantly inhibited in rats made hyperthyroid by L-thyroxine (T4) treatment. These results suggest that altered thyroid status influences GH release as well as TSH secretion induced by TRH in rats.

Animals↗
PubMed1976

Suppression by thyrotropin-releasing hormone (TRH) of growth hormone release induced by arginine and insulin-induced hypoglycemia in man.

Plasma growth hormone (GH) levels were significantly increased following L-arginine (30 g) infusion or insulin (0.1 U/kg body wt)-induced hypoglycemia in normal men. When synthetic thyrotropin-releasing hormone (TRH) (1 mg) was infused intravenously for 150 min, beginning 30 min before arginine or insulin administration, GH responses to arginine and insulin were significantly blunted with a mean (+/- SE) percentage inhibition of 80.1 +/- 8.8% and 30.6 +/- 10.3%, respectively. These results suggest a possible inhibitory effect of TRH on GH secretion in man.

Adult↗
PubMed1976

Effect of hypothalamic surgery on prolactin release induced by 5-hydroxytryptophan (5-HTP) in rats.

Intravenous injections of varying doses of 5-HTP (1, 3 and 5 mg/100 g body wt), a precursor of serotonin, caused a significant and dose-related increase in plasma prolactin concentrations in urethane-anesthetized rats. Increases in plasma prolactin concentrations caused by 5-HTP (1 mg/100 g body wt iv) were abolished by the concomitant administration of L-DOPA (2 mg/100 g body wt iv). Plasma prolactin levels were also significantly elevated following the injection of 5-HTP in rats with complete hypothalamic deafferentation, whereas 5-HTP had no significant effect on plasma prolactin levels in rats with extensive hypothalamic ablation. These results suggest that 5-HTP causes prolactin secretion by stimulating the serotoninergic mechanism in the hypothalamus.

5-Hydroxytryptophan↗
PubMed1976

Growth hormone release following thyrotrophin-releasing hormone injection into patients with anorexia nervosa.

The effect of thyrotrophin-releasing hormone (TRH) or luteinizing hormone-releasing hormone (LH-RH) on plasma levels of growth hormone (GH), prolactin (PRL), thyrotrophin (TSH), and luteinizing hormone (LHY, were studied in patients with anorexia nervosa. The basal plasma GH levels were elevated in 6 of 11 patients studied. Intravenous injection of synthetic TRH T500 mug) significantly raised the plasma GH levels in 9 of 11 patients. The peak values of plasma GH after TRH ranged from 6.0 to 31.5 ng/ml. Plasma GH concentrations also increased following the administration of synthetic LH-RH (100 mug) 1 of 7 patients. The intravenous injection of saline solution caused no significant change in plasma GH in these patients. The plasma LH responses to LH-RH were significantly blunted in all patients, whereas the plasma PRL and TSH responses to TRH were almost normal in the patients examined. These results suggest that the hypothalamo-pituitary function regulating GH and LH secretion is altered in patients with anorexia nervosa.

Adolescent↗
PubMed1976

Suppressive effect of L-dopa on human prolactin release during sleep.

Immunoreactive plasma human prolactin (HPr) and human growth hormone (HGH) concentrations were measured in six normal young men with polygraphic sleep monitoring during normal sleep and during sleep in which l-dihydroxyphenylalanine (l-DOPA) was infused intravenously at a rate of 0.8 to 1.0 mg/min. The intravenous infusion of l-DOPA significantly suppressed the episodic release of HPr during sleep and the occurrence of rapid eye movement (REM) sleep. However, HGH release during sleep was not remarkably influenced by l-DOPA. These results suggest that central catecholaminergic neural mechanisms are related to both sleep-related HPr release and REM sleep, but do not play an important role in sleep-related HGH release.

Adult↗
PubMed1975

Effects of drugs influencing brain catecholamines on GH release in rats with hypothalamic surgery.

The effect of pretreatment with alpha-methyl-p-tyrosine (alpha-MT) on the basal levels of plasma growth hormone (GH) and the responses to chlorpromazine (CPZ) were investigated in urethane-anesthetized rats with either complete hypothalamic deafferentation (c.d.), hypothalamic ablation (H.A.) or sham operation (Sham). Basal GH levels were high in C.D. rats, intermediate in H.A. rats, and low in Sham rats without any pretreatment. Pretreatment with alpha-MT caused a significant increase in basal GH levels in both C.D. and Sham rats, but not in H.A. rats. GH release following the intravenous injection of CPZ, which was observed in C.D. and Sham rats without alpha-MT pretreatment, was blunted by treatment with alpha-MT. In H.A. rats CPZ failed to stimulate the secretion of GH regardless of alpha-MT pretreatment. Neither the injection of L-DOPA nor DL-DOPS affected basal GH levels in non-alpha-MT pretreated C.D. rats. However, plasma GH levels significantly decreased following the injection of L-DOPA, but not DL-DOPS, in C.D. rats pretreated with alpha-MT. These findings suggest that the injection of CPZ causes an enhancement of GH release by inhibiting the catecholaminergic (dopaminergic) mechanism, which is active within the basal medial hypothalamus (BMH) and plays an inhibitory role in GH secretion. They also suggest that the extrahypothalamic inhibitory neural pathway, which is connected to the BMH and is interrupted by hypothalamic deafferentation, is not catecholaminergic.

Animals↗
PubMed1975

Pasma growth hormone responses to thyrotropin-releasing hormone in the urethane-anesthetized rat.

Intravenous injection of synthetic thyrotropin-releasing hormone (TRH) resulted in a significant and dose-related increase in plasma growth hormone (GH) in the urethane anesthetized rat. The minimum effective does of TRH was 40 ng per 100 g body wt when administered intravenously. The maximum responses of plasma GH to TRH were observed at 5 min following TRH, whereas those of plasma TSH were obtained at 10 min. Pretreatment with either T3 (50 mug/100 g body wt ip) significantly suppressed both plasma GH and TSH responses to TRH. The GH release induced by TRH was significantly inhibited by somatostatin (5 mug/100 g body wt iv) which was injected 5 min and immediately before the injection of TRH.

Anesthesia, General↗
PubMed1975

Growth hormone and prolactin release after injection of thyrotropin-releasing hormone in patients with depression.

The effects of thyrotropin-releasing hormone (TRH) on the release of growth hormone (GH), prolactin (PRL) and thyrotropin (TSH) were investigated in patients with depression. Intravenous injection of synthetic TRH (500 mug) caused a significant increase in plasma GH (peak value: 7.7 minus 35.0 ng/ml) in 8 of 13 patients with mental depression. After clinical recovery these patients had no response of plasma GH to TRH. TRH administration did not raise plasma GH in normal subjects examined. Plasma PRL responses to TRH were significantly enchanced (P smaller than 0.05) in depressed patients compared with control subjects. Plasma TSH responses to TRH were significantly blunted in patients with depression (P smaller than 0.05). These results suggest disorders in the hypothalamo-pituitary function in depression.

Adult↗
PubMed1975

Suppression by thyrotropin-releasing hormone (TRH) of human growth hormone release induced by L-dopa.

Oral administration of L-dopa (600 mg) significantly raised plasma human growth hormone (hGH) in 6 of 7 normal subjects examined. This L-dopa induced hGH release was significantly suppressed by the intravenous infusion of 1 mg of thyrotropin-releasing hormone (TRH). TRH administration alone had no significant effect on plasma hGH. In contrast, plasma human prolactin (hPRL) consistently increased following TRH infusion. L-dopa significantly lowered basal plasma hPRL levels and also significantly blunted TRH-induced hPRL release. These results suggest that TRH plays an inhibitory role in the regulation of hGH secretion in normal subjects, whereas it stimulates hPRL release.

Administration, Oral↗