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Biomedical subjects

K Chihara

Publications and source records attributed to K Chihara.

At least 361 records · Page 20Linked to original sources
PubMed1981

Regeneration of damaged ciliary epithelium in aphakic and pseudophakic eyes.

Mechanically damaged ciliary epithelium in aphakic and pseudophakic rabbit eyes was studied for up to 2 years after extracapsular lens extraction. Histopathological examination of the epithelium revealed more severe damage in pseudophakic eyes. The nonpigmented epithelium (NE) was missing from the middle to basal portion of each ciliary process. Regenerative ability of the NE was extremely poor. The damaged NE continued to disappear for at least 2 years, and only the pigmented epithelium (PE) covered the stroma. In some of the affected areas, the stroma of the ciliary body (CB) was substituted by fibrous materials.

Animals↗
PubMed1981

Effect of lithium on prolactin responses to thyrotropin releasing hormone in patients with manic state.

The plasma thyrotropin (TSH) and prolactin (PRL) responses to thyrotropin releasing hormone (TRH) were studied before and during lithium treatment for 3-4 weeks in 6 patients with manic states and 8 control subjects. The plasma TSH responses to TRH were not different between the two groups before lithium treatment. Lithium administration did not alter non-stimulated secretion of TSH in any groups, but resulted in exaggerated responses of plasma TSH to TRH in both groups. No difference between two groups was observed in plasma TSH responses to TRH. The basal plasma PRL concentration did not differ between the two groups and was not affected by lithium administration to either group. The plasma PRL responses to TRH in female subjects were greater than those in male subjects. In females, the plasma PRL responses to TRH in manic patients were significantly higher than those in control subjects before the treatment. Lithium administration caused enhanced responses to TRH in patients when compared to pretreatment levels, but not in control subjects. Although the small number of male subjects limits conclusions, pretreatment plasma PRL responses to TRH in male manic patients were apparently greater than those in control subjects. However, lithium administration appeared not to affect the responses of plasma PRL to TRH in manic patients when compared to pretreatment levels. The augmented responses of plasma PRL to TRH in patients with manic states suggest the existence of some abnormality in the hypothalamo-pituitary axis. Thus, the effect of the anti-manic agent on PRL secretion in manic patients may suggest the mechanism by which the drug affects manic symptoms.

Adult↗
PubMed1981

Effect of intraventricular injection of neurotensin and other various bioactive peptides on plasma immunoreactive somatostatin levels in rat hypophysial portal blood.

The role of various bioactive peptides in the control of secretion of hypothalamic somatostatin into the hypophysial portal blood was examined in anesthetized rats. Hypophysial portal blood was withdrawn at a rate of 5.0 microliter/min into a chilled tube through a cannula placed over the stump of the pituitary stalk and segmented every 20 min by air bubbles. Immunoreactive somatostatin (IRS) in the plasma was extracted with acetic acid and acetone and quantified by RIA. Basal levels (mean +/- SE) of plasma IRS in the hypophysial portal blood were 646 +/- 36 and 317 +/- 44 pg/ml in urethane- and pentobarbital-anesthetized rats, respectively. Under urethane anesthesia, injection of synthetic neurotensin into the lateral ventricle at various doses in the range of 0.016--2 microgram/rat caused a significant and dose-related increase of plasma IRS levels in the hypophysial portal blood, and this effect of neurotensin was significantly (P less than 0.05) suppressed by pretreatment with diphenhydramine (1 mg/100 g BW, iv), a histamine receptor blocker. Enhancement of IRS release by neurotensin was also observed in pentobarbital-anesthetized rats. Intraventricular injection of substance P (10 microgram/rat), beta-endorphin (1 and 5 microgram/rat), or [Met5]enkephalin had no effect on the level of somatostatin in the hypophysial portal blood of urethane-anesthetized rats. These results suggest a release of hypothalamic somatostatin into the hypophysial portal blood in response to intraventricular administration of neurotensin, probably by a histaminergic mechanism.

Animals↗
PubMed1981

Stimulation by bombesin of immunoreactive somatostatin release into rat hypophysial portal blood.

Bombesin was injected into the cerebral ventricle of male rats anesthetized with urethane to study its effect on plasma levels of immunoreactive somatostatin (IRS) in hypophysial portal and jugular blood. An intraventricular injection of bombesin (0.2 and 2 micrograms/rat) caused a significant and dose-related increase in plasma IRS in hypophysial portal blood but not in jugular blood. Although bombesin placed into the cerebral ventricle is known to stimulate glucagon and epinephrine release, an iv injection of glucagon (100 micrograms/100 g BW) or epinephrine (2.5 micrograms/100 g BW) did not cause any significant changes in plasma IRS levels in hypophysial portal and jugular blood, suggesting that these substances do not mediate bombesin stimulation of portal IRS release. Pretreatment with naloxone (75 micrograms/100 g BW, iv) failed to affect the portal IRS release induced by bombesin (2 micrograms/rat), indicating that the opiate receptor is not likely to be involved in this reaction. To ascertain whether IRS released by bombesin into hypophysial portal blood is biologically active, the effect of bombesin on the plasma GH level was then examined. Bombesin (2 micrograms/rat) injected intraventricularly completely suppressed the rise of plasma GH after the intraventricular injection of beta-endorphin (1 microgram/rat) or the iv injection of prostaglandin E1 (5 micrograms/100 g BW). Bombesin thus appears to stimulate the secretion of IRS, and probably biologically active somatostatin as well, from the hypothalamus into hypophysial portal blood, thereby inhibiting GH release from the anterior pituitary.

Animals↗
PubMed1981

Intraventricularly injected growth hormone stimulates somatostatin release into rat hypophysial portal blood.

The effects of GH on the release of somatostatin from the hypothalamus were assessed by measuring the concentrations of immunoreactive somatostatin (IRS) in hypophysial portal blood of urethane-anesthetized male rats. A significant and dose-related increase of IRS in hypophysial portal blood was observed during 20-80 min after a single injection of rat GH (5 and 25 micrograms) into the third ventricle. An intraventricular injection of ovine LH or vehicle alone did not affect IRS values in hypophysial portal blood. When rat GH was repeatedly injected into the cerebral ventricle at 75-min intervals, IRS in hypophysial portal blood rose following each injection in a similar pattern with a latency of 30-45 min. These findings suggest that the release of somatostatin from the hypothalamus is regulated, at least in part, by GH. Furthermore, in view of the inhibitory effect of somatostatin on GH secretion, stimulation by GH of somatostatin release into hypophysial portal blood may be involved in the mechanism by which GH regulates its own secretion.

Animals↗
PubMed1981

Concentration and secretion of gastric somatostatin in streptozotocin-diabetic rats.

Both the release and the content of gastric somatostatin were investigated in streptozotocin-diabetic rats. Fundic and antral somatostatin contents were both increased in streptozotocin-diabetic rats compared with control animals. Basal somatostatin levels in the perfusates of streptozotocin-treated animals were not significantly different from those of the control animals. However, the peak values of somatostatin release induced by 5 x 10(-9) M glucagon in the diabetic animals were significantly higher than those of the controls. These results lead us to conclude that a hyperfunctioning state of the gastric D-Cells exists in hypoinsulinemic diabetes.

Animals↗
PubMed1981

Reversal of increased gastric somatostatin in streptozotocin-diabetic rats by whole pancreas transplantation.

Changes in both the content and the release of gastric somatostatin after amelioration of streptozotocin (SZ)-induced diabetes by whole pancreas transplantation were investigated in the present study. Highly inbred male Lewis rats were divided into three groups: normal, control rats; SZ-induced diabetic rats; and SZ-diabetic rats after whole pancreas transplantation. Fundic as well as antral somatostatin content in the streptozotocin-diabetic rats was significantly increased compared with the controls. Whole pancreas transplantation in SZ-diabetic rats markedly lowered the increased somatostatin content both in the fundus and the antrum. On the other hand, the exaggerated somatostatin release induced by glucagon from the isolated, perfused stomach observed in the SZ-diabetic rats was reduced to the level of normal rats by whole pancreatic transplantation. From these results, it is concluded that the hyperfunction of gastric D-cells in the SZ-diabetic rats is reversed by transplantation of whole pancreas.

Animals↗
PubMed1981

Effect of antisomatostatin gamma-globulin on gastrin release in rats.

In order to determine the mechanism of endogenous gastric somatostatin in the regulation of gastrin release, antisomatostatin rabbit gamma-globulin was administered in vivo and in vitro in the rat. First, in rats anesthetized by chloral hydrate, intravenous injection of 1 ml antisomatostatin rabbit gamma-globulin had no significant effect on plasma gastrin levels. Second, basal gastrin release from the isolated perfused rat stomach was not affected by the administration of antisomatostatin rabbit gamma-globulin (1:99 and 1:1 dilutions). Third, the addition of antisomatostatin rabbit gamma-globulin (1:99) to incubated rat antral mucosa, however, significantly increased the basal gastrin release. From these results, it is concluded that antral somatostatin exerts its inhibitory effect on basal gastrin release mainly not through the circulation but via paracrine pathways.

Animals↗
PubMed1980

Effects of [Asu1,7]-eel calcitonin on gastric somatostatin and gastrin release.

Effects of [Asu1,7]-eel calcitonin on gastric somatostatin and gastrin secretion were studied by using the isolated perfused rat stomach. [Asu1,7]-eel calcitonin (10(-9)--10(-7)M) caused a simultaneous dose-dependent increase of gastric somatostatin release and decrease of gastrin secretion, with a significant correlation between these two. The demonstration of calcitonin stimulation of gastric somatostatin release raises the possibility of somatostatin-mediated suppression of gastrin secretion by calcitonin.

Animals↗
PubMed1980

Effects of various gastrointestinal peptides on gastric somatostatin release.

Effects of various gastrointestinal peptides on gastric somatostatin release from the isolated perfused rat stomach were studied. After isolation of the stomach in a fasted rat by the method of Lefébvre and preperfusion with 4.6% dextran-Krebs-Ringer bicarbonate buffer containing 5.5 mM glucose, each peptide was infused into the left gastric artery at a constant rate for 15 min. Secretin and bombesin caused a significant increase of gastric somatostatin release in a dose-related manner (10(-8)-10(-6) M). Gastric somatostatin release was also stimulated after the administration of pentagastrin (10(-8)-10(-6) M). In contrast, both methionine-enkephalin and substance P decreased gastric somatostatin release in a dose-related manner (10(-8)-10(-6) M), whereas neurotensin (10(-8)-10(-6) M) failed to change it significantly. The present results suggest that these various gastrointestinal peptides may regulate gastric somatostatin secretion.

Animals↗
PubMed1980

Clofibrate-induced myopathy in patients with diabetes insipidus.

Clofibrate has been considered to be a relatively safe antidiuretic in the treatment of diabetes insipidus. However, we have recently had four cases of clofibrate-induced myopathy in patients with diabetes insipidus due to hypothalamic lesions. Physicians should therefore be aware of its occurrence and carefully monitor serum levels of CPK, GOT and GPT during the treatment of diabetes insipidus with clofibrate, especially in patients with associated hypothyroidism, latent or overt, which possibly favors the development of myopathy.

Adolescent↗
PubMed1980

Effects of insulin and pancreatic polypeptide on gastric somatostatin release.

Effects of arginine and such pancreatic hormones as insulin and pancreatic polypeptide on gastric somatostatin release from the isolated perfused rat stomach were studied. The stomach was isolated from a fasted rat by a modification of the method of Lefébvre and was perfused with 4.6% dextran Krebs-Ringer biocarbonate buffer containing 5.5 mM glucose. Both insulin and pancreatic polypeptide (10(-10), 10(-9), and 10(-8) M) caused a significant decrease in gastric somatostatin secretion. Insulin (10(-10) M), furthermore, inhibited the glucagon (5 x 10(-8) M)-induced somatostatin response. Arginine (10 and 19 mM) failed to elicit any significant change of somatostatin release. These results suggest that gastric somatostatin release is affected by pancreatic hormones.

Animals↗