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Biomedical subjects

T Chiba

Publications and source records attributed to T Chiba.

At least 649 records · Page 36Linked to original sources
PubMed1981

[Maternal and fetal response to hemorrhagic anemia during organogenesis in rats].

The effects of artificial oligemic anemia on dams and their fetuses were investigated in pregnant rats. Animals divided into ten groups of four to six each were bled from the jugular vein at various stages of gestation. Hematological examination was performed on day 20 of gestation, then dams were sacrificed. Depression of maternal weight gain, decrease of food intake and increase of water intake were recognized in all the bled groups. These changes were more conspicuous in the groups venipunctured at early stages of organogenesis. At autopsy, there was no evidence of anemia in any of the groups bled before day 10 of pregnancy whereas the does bled after day 12 were found anemic. In term fetuses from these anemic mothers, however, no adverse findings suggestive of feto-toxicity and teratogenicity were noted.

Anemia↗
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↗
PubMed1981

Pre- and postsynaptic alpha-adrenergic effects of the antihypertensive drug budralazine.

Cardiac presynaptic and vascular postsynaptic alpha-adrenergic effects of 1-[2-(1,3-dimethyl-2-butenylidene)hydrazino]phthalazine (budralazine) were studied in comparison with those of hydralazine. Budralazine was about 3 times less potent than hydralazine in producing tachycardia in spontaneously hypertensive and normotensive rats when compared at equihypotensive doses. In normotensive pithed rats, budralazine at 3 mg/kg i.v. affected neither the tachycardiac response to cardioaccelerator nerve stimulation nor the inhibition of clonidine of the stimulation-induced tachycardia. As the dose was increased to 6 and 12 mg/kg i.v., however, budralazine not only inhibited transiently the sympathetic tachycardia but also enhanced the clonidine bradycardia, although this drug was almost without effect on resting heart rate. These effects of budralazine on the heart rate response in the stimulated rats were partially but significantly antagonized by pretreatment with phentolamine. Hydralazine (3 mg/kg i.v.) differed from budralazine in that its transient inhibition of the stimulation-induced tachycardia was not modified by phentolamine and it produced an acceleration of the recovery of clonidine bradycardia as well as an increase in resting heart rate. Budralazine (3--12 mg/kg i.v.), like hydralazine (0.3 and 3 mg/kg i.v.), antagonized pressor responses to noradrenaline and phenylephrine but did not affect the tachycardia produced by both agonists in normotensive pithed rats. Based on these results, a possible mechanism of hypotensive and weak tachycardiac actions of budralazine is discussed in relation to that of hydralazine.

Animals↗
PubMed1981

Antihypertensive and general pharmacological properties of budralazine.

Antihypertensive and general pharmacological properties of 1-[2-(1,3-dimethyl-2-butenylidene)hydrazino]phthalazine (budralazine) were studied in comparison with those of hydralazine. Single oral administration of budralazine (4--15 mg/kg) to DOCA/saline hypertensive rats resulted in a dose-related and sustained antihypertensive effect which was 2--3 times less potent than that of hydralazine. However, there were no remarkable differences between both drugs in the hypotensive magnitude after the 4-week treatment of spontaneously hypertensive rats (SHR) with their higher doses. After single oral administration, budralazine was about 8 times less potent than hydralazine in increasing plasma renin activity in normotensive rats. At effective antihypertensive doses, budralazine inhibited spontaneous motor activity (mice), gastrointestinal propulsion (mice), gastric emptying rate (rats), gastric secretion (rats), urine output and urinary electrolyte excretion (rats) as well as carrageenan-induced paw edema formation (rats), which were essentially less potent than those produced by hydralazine. Budralazine at 6 mg/kg i.v. exhibited a slowing of neocortical EEG (cats) and a slight increase in spinal monosynaptic potentials (cats) and inhibited gastrointestinal motility (dogs). The same dose of hydralazine produced an increase in occurrence of the neocortical fast waves, an inhibition of the monosynaptic potentials and the carotid sinus reflex (dogs) and a stimulation of intestinal motility followed by prolonged and marked reduction. Budralazine (10(-5) g/ml) slightly potentiated contractile response of isolated guinea-pig vas deferens to noradrenaline, whereas hydralazine (10(-4) g/ml) inhibited the response. Budralazine (10(-5) g/ml), like hydralazine (10(-4) g/ml), produced a nonspecific antagonism against the contractile response of isolated guinea-pig ileum to various spasmogens, and both drugs (10(-4) g/ml) reduced either spontaneous motility or oxytocin-induced motility in isolated rat uterus.

Animals↗
PubMed1981

[Histochemical study on the denervated and reinnervated muscle of the rat (author's transl)].

Distribution of white and red muscle fiber is well demonstrated by means of enzyme histochemistry as a mosaic pattern. Nervous control on both different type of fibers is still obscure. In order to elucidate this problem, an experiment of denervation was carried out on the rat. The sciatic nerve was resected at sciatic notch for a distance of one cm. The extensors of lower leg were examined on histochemical preparation using succinate dehydrogenase activity staining at intervals following denervation. A tendency of faster atrophy of white fibers in the relatively superficial layer than red fibers was noted. Enzyme activity decreased gradually in both fibers. At about eight weeks reinnervation began to occur at the deeper layer near the motor point. Reinnervated large fibers appeared with a tendency of cluster formation with the enzyme as red fibers. It is suggested that fiber type is dependent on the nervous control.

Animals↗
PubMed1980

Hysteria and urbanization.

The statistics of neuropsychiatric clinics in two general hospitals in Sendai City were analyzed to investigate the relation between the incidence of hysteria and the urbanization in terms of population density. The proportion of hysteric women to total female patients had decreased in both clinics in recent years. The incidence of hysteric patients seemed to decrease in almost all population sizes of their residential administrative units except for in a couple of population sizes. The incidence of hysteric patients was relatively high in the satellites of the Sendai metropolis. It might be a loss of traditional sociocultural ties in the urbanizing process that increases the risk of hysteria.

Adolescent↗
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

Somatostatin release from the isolated, perfused diabetic rat pancreas: inverse relationship between pancreatic somatostatin and insulin.

The changes in pancreatic somatostatin content and release were studied in streptozotocin (STZ)-diabetic rats. Male Wistar rats were treated with a graded dose of STZ (group I, 0; II, 25; III, 50; IV, 75 mg/kg), which produced various grades of diabetic rats four weeks later. The pancreatic somatostatin content increased in proportion to the dose of STZ (I, 189 +/- 31; II, 222 +/- 20, III, 343 +/- 4; IV, 515 +/- 36 ng/g wet wt), while graded reductions of insulin content were observed. Significant increases in glucagon content were found only in groups III and IV. Pancreatic somatostatin release increased during arginine infusion (19.2 mM) dose dependently, (I, 543 +/- 36; II, 946 +/- 64; III, 1229 +/- 55; IV, 2186 +/- 150 pg/15 min), and it correlated with the graded decreases of insulin release. The glucagon release induced by arginine, however, did not change significantly. These results indicate that pancreatic somatostatin content and release increased in STZ-diabetic rats in proportion to the degree of insulin deficiency.

Animals↗