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T Ichihara

Publications and source records attributed to T Ichihara.

At least 163 records · Page 9Linked to original sources
PubMed1989

Effects of Bay K 8644 on renal function and renin secretion in anesthetized rats.

Our previous study on kidney cortical slices showed that Bay K 8644, a dihydropyridine calcium channel agonist, produced a dose-dependent inhibitory action on the release of renin. The present study was performed to examine the effect of Bay K 8644 on renal function and renin secretion in vivo. When Bay K 8644 was directly infused into the renal artery of anesthetized rats, 2 micrograms/kg/min had no effect on renal blood flow (RBF) and glomerular filtration rate (GFR), but decreased urine flow (UF), urinary sodium excretion (UNaV) and fractional sodium excretion (FENa) by about 30%, 55% and 35%, respectively, thereby suggesting that Bay K 8644 enhanced the tubular reabsorption of water and sodium. When 10 micrograms/kg/min were infused, RBF, GFR, UF, UNaV and FENa decreased to about 95%, 70%, 35%, 35% and 30% of each control value. The administration of Bay K 8644 at 10 micrograms/kg/min did not influence the basal levels of plasma renin activity (PRA) and renin secretion rate (RSR), but did inhibit significantly isoproterenol-induced increasing effects on PRA and RSR. These results indicate that the activation of voltage-dependent calcium channels with Bay K 8644 influences the control of renal function and renin secretion in vivo.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1989

Clinicohistopathologic and immunohistochemical studies of intrapancreatic development of carcinoma of the head of the pancreas.

Clinicohistopathologic and immunohistochemical studies of intrapancreatic development of duct cell carcinoma of the head of the pancreas to the body and tail were done in 34 cases in which total pancreatectomy accompanied by portal vein resection were performed from July 1981 to June 1987. In studies of hematoxylin and eosin (HE) staining, intrapancreatic development from the head to the body or tail was observed in 14 cases of 34 cases (41.1%). Multicentricity or skip development was observed in two of 14 cases. However, by using immunostaining of carcinoembryonic antigen (CEA), carbohydrate antigen 19-9 (CA19-9) and DUPAN2, small cancer nests surrounded by dense fibrous connective tissues could be easily and accurately diagnosed, and finally, in 25 of 34 cases (73.5%), intrapancreatic continuous development from the head to body or tail was observed. The intrapancreatic development correlated with portal invasion and perineural invasion of carcinoma, hardness of body and tail, obstruction of the main pancreatic duct, and irregular pancreaticogram. The intraoperative quick immunostaining on the cryostat sections, together with HE staining, is useful to determine the intrapancreatic development of the carcinoma. The indication of total pancreatectomy or pancreatoduodenectomy for carcinoma of the head of the pancreas can be determined by these results.

Adenoma, Islet Cell↗
PubMed1989

Inhibitory effect of nisoldipine on angiotensin-II-induced renal actions in anesthetized dogs.

Renal effects of nisoldipine, a potent calcium channel blocker, were examined in anesthetized dogs. Intrarenal arterial infusion of nisoldipine (2, 10, and 50 ng/kg per min) had no effect on mean systemic blood pressure and heart rate and there was no significant change in renal hemodynamics during infusion of various doses of the drug. Urine flow and urinary excretions of sodium, chloride, and potassium were increased by nisoldipine in a dose-related manner. Fractional excretions of sodium and chloride were markedly elevated with the highest dose given thereby indicating that tubular reabsorptions of sodium and chloride were inhibited by nisoldipine. Nisoldipine (50 ng/kg per min) abolished the decreasing effects of angiotensin-II on glomerular filtration rate, urine flow, and urinary excretion of electrolytes but not the decrease in renal blood flow by the peptide. Angiotensin-II-induced reduction of fractional excretion of electrolytes was completely blocked by nisoldipine. Renal responses to norepinephrine were unaffected by nisoldipine. Thus, nisoldipine administered intrarenally to anesthetized dogs exerts a diuretic action by way of tubular effects, as is the case with other dihydropyridine calcium channel blockers. Nisoldipine seems to effectively antagonize the renal response to angiotensin-II. Thus, the preferential inhibition of angiotensin-II-induced antidiuresis may mean that nisoldipine interferes with stimulatory effects of angiotensin-II on the renal tubular reabsorption of electrolytes and water.

Anesthesia↗
PubMed1989

Inhibitory effect of peptide YY on gastric acid output in rats.

The administration of peptide YY (PYY: 0.8, 1.6 and 3.2 nmol/kg/h, i.v.) to fasting rats inhibited not only baclofen (2 mg/kg, s.c.)-stimulated gastric acid output and gastric mucosal blood flow, but also pentagastrin (8 micrograms/kg/h, i.v.)-stimulated gastric acid output. PYY (3.2 nmol/kg/h) reduced baclofen-induced acid output more than pentagastrin-induced acid output, i.e., by 61.8 +/- 11.5% compared to 35.3 +/- 8.2%. PYY inhibited acetylcholine (ACh) release from cholinergic nerve endings of gastric body evoked by electrical transmural stimulation (ETS: 1 msec, 10 V, 3 Hz, 30 sec) by 47.2 +/- 3.5%. The mechanism of the inhibitory effect of PYY on gastric acid output seems to involve decreased gastric mucosal blood flow and reduced ACh release from cholinergic nerves.

Animals↗
PubMed1989

The mechanism of acute gastric ulcer after induced hemorrhagic shock.

Changes in gastric mucosal blood flow were investigated for their relationship to gastric mucosal prostaglandin E2 (PGE2) and noradrenaline (NA) in rats with hemorrhagic shock. The results were as follows: 1) Gastric mucosal blood flow and NA decreased after hemorrhage. Gastric mucosal PGE2 initially increased after exsanguination and then markedly decreased. 2) Administration of NA before hemorrhage resulted in an increase of PGE2. However, the PGE2 value for animals receiving NA after hemorrhage was not different from that of non-NA-treated group. 3) Pre-treatment with PGE2 suppressed the reduction in both gastric mucosal blood flow and NA and the development of ulcer. These results suggest that the increase in gastric mucosal PGE2 in the early stage of shock might represent a phenomenon of adaptation by the adrenergic activation, and the decrease in PGE2 in the late stage might result from impaired synthesis of PGE2 due to persistent hypoxia and might be one of the possible factors in ulcer formation.

Acute Disease↗
PubMed1989

[The effect of cimetidine to suppress the reduction of gastric mucosal blood flow caused by immobilization in water--its relationship to noradrenaline].

Reduction of gastric mucosal blood flow has been regarded as being the most important event for the gastric defensive mechanisms. In male Wistar rats immobilized in water, the authors recently studied the effect of cimetidine on the gastric mucosal blood flow and the mechanism for that action of cimetidine. In vivo, animals were divided into four groups (PGE2-treated, PGI2-treated and cimetidine-treated groups and an untreated control group), and mucosal blood flow before and 4 hours after the start of immobilization was determined with the electrolytic hydrogen gas clearance technique. In vitro involving perfusion of the isolated gastric blood vessels, the effect of treatment with PGE2, PGI1 or cimetidine in the presence of stimulation with noradrenaline was assessed. The stress-caused blood flow reduction was significantly suppressed in the PGE2-treated group (26.9% reduction in blood flow), the PGI2-treated group (15.7%) and also in the cimetidine-treated group (39.2%) as compared to the controls in which blood flow was reduced by 58.0% following immobilization. In vitro, cimetidine treatment resulted in a reduction of gastric perfusion pressure by 36.6% at maximum although the reduction was more marked following treatment with PGE2 (44.9% reduction) or PGI2 (49.4%). This result suggests that cimetidine also has a vasodilative action.

Animals↗
PubMed1989

[Measurement of superoxide dismutase activity in normal skin by electron spin resonance-spin trapping method].

Superoxide dismutase (SOD) activity in 20 skin specimens from healthy individuals measured by the electron spin resonance-spin trapping method was 7.08 U +/- 0.41 U/mg protein (mean +/- SE). This method may be useful in the determination of SOD, since it requires a shorter time (approx. 3 min) and a smaller amount of specimen (approx. 30 mg) than previously reported methods other than the EIA method.

Adolescent↗
PubMed1989

[Pathological features and treatment of ulcerative lesions of the duodenum associated with Crohn's disease].

Among a total of 22 patients with Crohn's disease, eight patients with duodenal ulcerative lesions were investigated for pathological features and treatment. All duodenal ulcerative lesions of the eight patients were difficult to be distinguished morphologically from peptic duodenal ulcers at the beginning. But during the course of observation six of eight lesions revealed different pathological features from peptic duodenal ulcers: One showed highly edematous mucosa. Four granular mucosa, and another one longitudinal ulcers and cobblestone appearance. Gastric analysis of these patients showed 6.6 +/- 4.0 mEq/L of BAO and 21.3 +/- 3.4 mEq/L of MAO which was comparable to high acidity of peptic duodenal ulcers. Effectiveness of administration of anti-peptic ulcer drugs only and both anti-peptic ulcer drugs plus drugs against Crohn's disease were 40.0% and 57.1%, respectively. Two patients underwent distal partial gastrectomy. Recurrence was not observed. In conclusion, high acidity would be a cause of duodenal ulcerative lesions associated with Crohn's disease, and the pathological features of them would be affected by Crohn's disease itself. Anti-peptic ulcer drugs should to be administered as well as drugs against Crohn's disease. The method which has hypoacidity effect should be selected in operative therapy to such patients as to have stenosis of the duodenum.

Adolescent↗
PubMed1989

[Study of complications after endoscopic sclerotherapy for esophageal varices--particularly 2 cases that changed portal circulation after sclerotherapy].

In 116 patients with esophageal varix due to liver cirrhosis who received the endoscopic sclerotherapy, the following complications were observed after the sclerotherapy: 38 ulcer formation; 19 chest pain; 16 hypotension; 15 fever; 12 pleural effusion; 6 esophageal stenosis and so on. Furthermore, two cases with marked changes of portal circulation were experienced after the sclerotherapy. The first case had severe bleeding out of duodenal varix four months after the sclerotherapy and died because of massive bleeding. The second case had hepatic encephalopathy six months after the sclerotherapy. In both cases, angiography revealed the development of collateral veins after the sclerotherapy. Because the abrupt intercept of the esophageal varix by the successful sclerotherapy causes the increase of the other collateral blood flow, the changes of portal circulation must be watched carefully afterward.

Adult↗
PubMed1988

Immunohistochemical localization of CA 19-9 and CEA in pancreatic carcinoma and associated diseases.

The distribution of carbohydrate antigen 19-9 (CA 19-9), on pancreatic carcinomas and associated diseases correlated with carcinoembryonic antigen (CEA) localization is described. Immunohistochemical examinations were made on pancreatic specimens from 45 patients with pancreatic carcinoma. In normal pancreatic duct, the antigens were restricted to the luminal surface. In some hyperplastic epithelium, however, they were localized not only to the basolateral plasma membranes but also to the cytoplasm. In neoplastic glands, the antigens were distributed over the entire surface of the cells and in the surrounding stroma adjacent to the basal membranes of the malignant cells. The findings were compatible with previous observations of CEA and secretory component (SC) localization in gastric and colonic mucosa. In addition, the staining intensity of CA 19-9 in the routine formalin-fixed and paraffin-embedded sections was much superior to that of CEA. The relationship between CA 19-9 and other blood group antigens, such as Lewis a and Lewis b, also was discussed. Localizations of these antigens in pancreatic tissues are useful for the biologic analysis of abnormalities of the pancreatic duct epithelium, and may well facilitate pathologic diagnosis of pancreatic carcinoma.

Antigens, Neoplasm↗
PubMed1988

Stimulatory effects of neuronally released norepinephrine on renin release from rat kidney cortical slices.

Stimulatory effects of extracellular high K+ in the presence of nifedipine (NIF) on renin release (RR) from kidney cortical slices were investigated. The stimulation was suppressed either by propranolol or by metoprolol but not by prazosin. High K+ plus NIF-induced increase in RR was attenuated by renal denervation. The enhancing effect was not observed when the slices were incubated in Ca2+-free buffer or in medium containing divalent cations such as Cd2+, Co2+ and Mn2+. These alterations in RR correlated with 3H-efflux from the slices preloaded with 3H-norepinephrine. We conclude that the high K+ plus NIF-induced increase in RR from the slices is mediated by norepinephrine (NE) derived from renal sympathetic nerves and that this neuronally released NE stimulates RR via the activation of beta-adrenoceptors.

Animals↗
PubMed1988

Calmodulin-independent stimulation of renin release by exposure of rat kidney cortical slices to calcium.

1. Effects of calcium-interacting agents on the calcium-induced stimulation of renin release from kidney cortical slices pretreated with calcium-free medium were examined. 2. The exposure of calcium to the slices pretreated with calcium-free medium enhanced the release of renin, followed by a decreased response in the release. The amount of lactate dehydrogenase released from the slices did not correlate with that of renin. 3. High potassium depolarization significantly potentiated the decreased response of renin release, with no influence on the stimulation of the release by exposure to calcium. 4. The decrease in renin release was attenuated by calcium-interacting agents, such as nifedipine, TMB-8 and W-7, but these agents were without effect on the stimulation of the release by exposure to calcium. 5. Thus, the calcium-calmodulin system apparently is not involved in the increased response of renin release following exposure to calcium.

Angiotensin I↗
PubMed1988

Stimulatory effects of neuronally released norepinephrine on renin release in vitro.

Extracellular high potassium inhibits renin release in vitro by increasing calcium concentrations in the juxtaglomerular cells. We found that the decreased response of renin release from rat kidney cortical slices in high potassium solution (20-80 mM) changed to a strikingly increased one in the presence of nifedipine at doses over 10(-6) M. We then examined the stimulatory effect of extracellular high potassium in the presence of nifedipine on renin release. The enhancement of release was significantly suppressed either by propranolol or by metoprolol but not by prazosin. High potassium plus nifedipine-induced increase in renin release was markedly attenuated by renal denervation. The enhancing effect was not observed when the slices were incubated in calcium-free medium. Divalent cations such as Cd2+, Co2+, and Mn2+ (0.1-3.0 mM) blocked this enhancement in a concentration-dependent manner. High potassium elicited an increase in 3H efflux from the slices preloaded with [3H]norepinephrine. The increasing effect was not influenced by nifedipine but was abolished by the removal of extracellular calcium or by the addition of divalent cations. These observations suggest to us that the high potassium plus nifedipine-induced increase in renin release from the slices is mediated by norepinephrine derived from renal sympathetic nerves and that this neuronally released norepinephrine stimulates renin release via activation of beta-adrenoceptors.

Animals↗
PubMed1988

High serum levels of DUPAN2 antigen and CA19-9 in pancreatic cancer: correlation with immunocytochemical localization of antigens in cancer cells.

We determined the concentration of serum DUPAN2 and CA19-9 in 43 pancreatic cancer patients by enzyme immunoassay, and compared the staining patterns of the antigens in the tissues of pancreatic cancer in order to clarify the mechanism of the elevation of serum DUPAN2 and CA19-9 levels in the patients. In 26 patients (60%), the serum DUPAN2 concentration was higher than 300 U/ml. This positive rate was not so high as that of CA19-9. However, seven out of the twelve CA19-9-negative patients were DUPAN2-positive. Using a combined assay of serum DUPAN2 and CA19-9, the diagnostic sensitivity for pancreatic cancer was 88% (38/43). Immunocytochemically, both DUPAN2 and CA19-9 were restricted to the apical surface and/or supranuclear cytoplasm in the normal pancreatic duct epithelia. In cancerous glands, however, the two were found over the entire surface and cytoplasm of the cancer cells--losing the polar distribution pattern of the antigen--and in the surrounding stroma adjacent to the cancer cells. DUPAN2 was detected in 47 (89%) out of 53 adenocarcinomas of the pancreas, and CA19-9 in 44 cases (83%). Cases with high serum antigen levels tended to display high proportions of stromal staining in the cancer tissues. These findings suggest that shedding of the antigen into the stroma adjacent to the malignant glands is one of the major mechanisms in the elevation of high serum DUPAN2 and CA19-9 levels.

Adenocarcinoma↗
PubMed1987

Renin release in anesthetized rats is enhanced by the calmodulin antagonist W-7.

In foregoing work, we found that the release of renin from rat kidney cortical slices was stimulated by the calmodulin antagonist W-7. The present work was done to determine whether W-7 would stimulate renin release in vivo. W-7 and its control agent, W-5 were directly infused into the renal artery of anesthetized rats. W-7 and W-5, at 50 micrograms/kg/min, produced no significant effects on renin release. Infusion of W-7 at 100 micrograms/kg/min resulted in a marked stimulation of renin release, but there was no significant alteration in the release when the same dose of W-5 was infused. Both compounds elicited a slight decrease in renal blood flow. The alterations in renin release and renal blood flow seen with W-7 were not affected by pretreatment with phentolamine or propranolol. As W-7 stimulates renin release in vivo, the hypothesis that Ca2+-calmodulin plays an inhibitory role in renin release from the kidney is given added support.

Animals↗
PubMed1987

[Clinicohistopathological and immunohistochemical studies on intrapancreatic spread of pancreatic carcinoma].

Clinicohistopathological and immunohistochemical studies on intrapancreatic spread of pancreatic carcinoma were performed on 30 cases with total pancreatectomy accompanied by portal vein resection. In the observation of HE stained tissue sections of 25 cases of carcinoma of head of the pancreas, the intrapancreatic spread from the head to body or tail was observed in 9 out of 25 cases (36%). However, by the immunostaining of CEA, CA19-9 and Dupan 2, small cancer nests surrounded by fibrous tissues could be easily detected and intrapancreatic continuous spread from the head to body or tail was observed in 15 out of 25 cases (60%). The intrapancreatic spread of the carcinoma correlated with portal invasion of carcinoma, hardness of the body and tail, obstruction of main pancreatic duct and irregular pancreaticogram. The intraoperative quick immunostaining on the cryostat sections of the pancreatic tissue, together with the HE staining, is useful to determine the intrapancreatic spread of the carcinoma. The indication of total pancreatectomy for pancreatic carcinoma can be determined by these results.

Antigens, Neoplasm↗