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Biomedical subjects

K Chihara

Publications and source records attributed to K Chihara.

At least 379 records · Page 21Linked to original sources
PubMed1980

Effects of glucagon, secretin, and vasoactive intestinal polypeptide on gastric somatostatin and gastrin release from isolated perfused rat stomach.

To investigate the role of gastric somatostatin on gastrin secretion, glucagon, secretin, and vasoactive intestinal polypeptide (VIP) were perfused in the isolated pancreas-spleen-duodenum deprived preparation of rat stomach. After a preperfusion with 4.6% dextran Krebs-Ringer bicarbonate buffer containing 5.5 mM glucose, glucagon, secretin, and VIP at the concentrations of 10(-8), 10(-7), and 10(-6) M were infused into the left gastric artery at a constant flow of 2 ml/min for 15 min. All glucagon, secretin, and VIP evoked dose-dependent increases of somatostatin secretion with a simultaneous dose-related decrease of gastrin release. Furthermore, a significant correlation was found between the increase of somatostatin release and the decrease of gastrin secretion induced by glucagon, secretin, and VIP. These results raise the possibility that the suppression of gastrin secretion induced by glucagon, secretin, and VIP may, at least in part, be mediated by local action of gastric somatostatin.

Animals↗
PubMed1979

Enhancement of immunoreactive somatostatin release into hypophysial portal blood by electrical stimulation of the preoptic area in the rat.

Electrical stimulation of the preoptic area resulted in a significant increase in the secretion rate of immunoreactive somatostatin (IRS) and its concentration in the hypophysial portal blood of urethane-anesthetized rats. In contrast, stimulation of the ventromedial nucleus did not cause any changes in portal immunoreactive somatostatin. The flow rate of portal blood also increased significantly by electrical stimuli to the preoptic area but not to the ventromedial hypothalamus. These findings support the view that the preoptic area plays an inhibitory role in the regulation of GH secretion by increasing the release of somatostatin into hypophysial portal vessels in the rat.

Animals↗
PubMed1978

Effect of intraventricular administration of anti-somatostatin gamma-globulin on the lethal dose-50 of strychnine and pentobarbital in rats.

Effects of intraventricular injection of sheep anti-somatostatin gamma-globulin (anti-SSG) on strychnine-induced seizures, strychnine LD50, and pentobarbital LD50 were examined in male rats under light ether anesthesia. Ten microliters of anti-SSG given 2 h earlier significantly decreased the duration of strychnine-induced seizures as compared with that in the control rats pretreated with normal sheep gamma-globulin (NSG). This effect of anti-SSG seemed to be specific, as there was no difference in seizure duration between sheep anti-LHRH gamma-globulin (anti-LHRHG)- and NSG-pretreated rats. Survival rates in anti-SSG-pretreated rats after injection of strychnine and pentobarbital were significantly larger (P less than 0.01 and P less than 0.05, respectively) than those in the control rats receiving NSG. The administration of anti-SSG resulted in 26.7% and 22.9% increases in the LD50 of strychnine and pentobarbital, respectively. These results indicate that endogenous somatostatin in the cerebrospinal fluids and/or the periventricular tissue nodulates the response of the central nervous system to strychnine and pentobarbital in rats.

Animals↗
PubMed1978

Studies on the mechanism of growth hormone and thyrotropin responses to somatostatin antiserum in anesthetized rats.

An iv administration of 1 ml sheep antiserum to somatostatin (anti-SS) resulted in marked increases of both serum GH and TSH, with a peak 10--20 min after administration in male rats anesthetized with urethane or pentobarbital. Administration of anti-SS had no effect on serum PRL. Ablation of the basal medial hypothalamus abolished the rises of both serum GH and TSH after anti-SS administration. Intravenous injection of 1 ml rabbit antiserum to TRH (anti-TRH) decreased serum TSH levels 15 min after injection, whereas injection of normal rabbit serum did not affect TSH levels. Serum TSH levels did not rise after injection of anti-SS in rats pretreated with anti-TRH. On the other hand, pretreatment with anti-TRH did not affect the basal serum GH levels nor the anti-SS-induced GH release. The enhanced secretion of GH and TSH after anti-SS injections was not blocked by pretreatment with indomethacin, an inhibitor of prostaglandin synthesis. The following conclusions were made: 1) both GH and TSH responses to anti-SS require an intact basal medial hypothalamus; (2) TSH response to anti-SS is mediated by hypothalamic TRH; and 3) the GH response may be mediated by hypothalamic GH-releasing hormone which is not TRH or prostaglandins.

Anesthesia↗
PubMed1977

Sleep-related growth hormone release following 2-bromo-alpha-ergocriptine treatment in acromegalic patients.

Plasma growth hormone (GH) concentrations were measured over 24 h in seven acromegalic patients before and during treatment with 2-bromo-alpha-ergocriptine (CB-154). Before treatment basal plasma GH levels were consistently elevated but no significant change was observed between the mean plasma GH levels during sleep and during waking in five of the seven patients examined. The daily administration of CB-154 (5 to 10 mg, orally) for 14 days resulted in a significant fall in the 24 h mean plasma GH levels in six of the seven patients. In all of the six patients who responded to CB-154 treatment, the mean plasma GH concentrations during sleep were significantly greater than during waking. Daytime sleep was associated with a significant rise in plasma GH in both of the two patients examined. It is concluded that CB-154 treatment resulted in a significant decrease in plasma GH levels with sleep-related increase in some acromegalics although the mechanism responsible for this sleep-related GH rise remains to be further investigated.

Acromegaly↗
PubMed1977

Effects of thyrotropin-releasing hormone on sleep and sleep-related growth hormone release in normal subjects.

Effects of TRH on sleep and sleep-related growth hormone (GH) release were examined in four normal volunteers. A bolus of 500 microgram of synthetic TRH was injected iv at the onset of sleep, followed by continuous iv infusion of 1000 microgram of TRH dissolved in saline for 3 h on two nights. Saline alone was infused on two control nights in each of these subjects. Polygraphic sleep records showed that TRH transiently interrupted sleep on both nights in all of the four subjects. The arousal phenomenon was observed from 80 to 151 min after the start of TRH administration until 20 to 212 min after the end of TRH infusion. The mean (+/-SE) percentage of awakening on the nights of TRH administration was significantly larger than on the control nights (36.4 +/- 1.9% vs. 1.3 +/- 0.8%, P less than 0.001). Plasma GH increased in close relationship to the initial appearance of slow wave sleep (SWS) within 40 min after sleep onset on both control nights in all four subjects. On nights of TRH administration, however, plasma GH levels during the initial 80 min of sleep were significantly lower (P less than 0.005) than on control nights, whereas SWS was demonstrated before the interruption of sleep. On nights when sleep was interrupted by forced wakefulness 1 h after sleep onset, plasma GH rose to levels comparable to those on control nights during early sleep periods in all subjects examined. These results suggest that TRH inhibits sleep and sleep-related GH release in normal subjects.

Adult↗
PubMed1977

Growth hormone release by gamma-aminobutyric acid (GABA) and gamma-amino-beta-hydroxybutyric acid (GABOB) in the rat.

Effects of gamma-aminobutyric acid (GABA) and gamma-amino-beta-hydroxybutyric acid (GABOB) on growth hormone (GH) release were investigated in the urethaneanesthetized male rat. An intraventricular injection of GABA and L-GABOB but not D-GABOB caused a significant increase in plasma GH. An intravenous injection of L-GABOB, at the dose which had no significant effect on basal plasma GH, remarkably enhanced plasma GH response to pentobarbital. These results suggest that GABA and L-GABOB stimulate GH release possibly via the central nervous system in the rat.

Aminobutyrates↗