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Biomedical subjects

S Okabe

Publications and source records attributed to S Okabe.

At least 469 records · Page 26Linked to original sources
PubMed1984

Comparative study of hydrogen and aminopyrine clearance methods for determination of gastric mucosal blood flow in dogs.

Effects of pentagastrin, histamine, PGI2, and vasopressin on gastric mucosal blood flow (GMBF) in innervated stomaches of anesthetized dogs were measured by means of the hydrogen clearance method, using a contact electrode. The results were compared with findings obtained with the aminopyrine (AP) clearance method in Heidenhain pouch preparations. Pentagastrin at 2 and 8 micrograms/kg/hr had no effects on GMBF, as measured by the hydrogen clearance method, but there was a marked increase in GMBF when the AP clearance method was used. Histamine at 40 or 160 micrograms/kg/hr tended to reduce or significantly reduced GMBF when measured with the hydrogen clearance method, but there was a significant increase in GMBF with the AP clearance method. Both PGI2 (3 or 30 micrograms/kg/hr) and vasopressin (0.06 or 0.25 units/kg/hr) reduced GMBF as determined by both methods. These results indicate that the hydrogen clearance method is advantageous for detecting regional GMBF but is disadvantageous when attempting to detect the effects of agents which increase GMBF.

Aminopyrine↗
PubMed1984

Role of lymphoid nodules in pathogenesis of indomethacin-induced gastric lesions in dogs.

Pathogenesis of indomethacin-induced gastric lesions in beagles was studied morphologically. While a single oral administration of indomethacin (20 mg/kg) did not induce visible lesions in the stomach of male beagles, repeated administration once daily for 5 or 10 days induced gastric erosions or ulcers, mainly in the antrum. When this compound was given once or repeatedly, histological examination showed that the total number of lymphoid nodules both in the fundus and antrum tended to increase or significantly increased. The number of large nodules (over 350 micron in diameter) was significantly increased, particularly in the antrum. Some of these enlarged nodules seen at the surface of the mucosa showed damage at the luminal area, and the lesions were microscopically visible. Indomethacin is known to disrupt the gastric mucosal barrier in dogs, leading to increased back-diffusion of acid. Our findings and those of others suggest that indomethacin may induce lesions in specific portions of the dog stomach, initiated by enlargement of lymphoid nodules followed by damage to some of these nodules, probably due to a corrosive effect of gastric juice through the disrupted mucosal barrier.

Administration, Oral↗
PubMed1984

Effects of FPL-52694, a new mast cell stabilizer, on gastric secretion and various acute gastric lesions in rats.

Oral FPL-52694 [5-(2-hydroxypropoxy)-8-propyl-4-oxo-4H-1-benzopyran-2-carboxylic acid Na], a new mast cell stabilizer, dose-dependently inhibited gastric acid secretion but increased the volume and pepsin output in pylorus-ligated rats. Intraduodenal FPL-52694 significantly inhibited all of the volume, acidity, acid output and pepsin output. Concerning the acidity, oral administration of the agent showed much more potent inhibition than intraduodenal administration. Oral FPL-52694 markedly inhibited the development of pylorus-ligated ulcers, water-immersion stress- and aspirin-induced gastric erosions and moderately inhibited the formation of reserpine-induced gastric erosions in rats. Intraduodenal FPL-52694 also inhibited pylorus-ligated ulcers whereas it had no effect on aspirin-induced gastric erosions. Histamine-induced gastric erosions were not affected by oral FPL-52694. These effects of FPL-52694 were almost the same as those of cimetidine, except that cimetidine tended to inhibit histamine-induced gastric erosions. Although the precise mechanism of action of FPL-52694 remains unknown, oral FPL-52694 appears to be a promising agent for the treatment of peptic ulcers.

Animals↗
PubMed1984

Time variation of radon daughters concentration in snowfall.

Time variation of radon daughters concentration in snowfall was measured continuously. The relations of radon daughters concentration in snowfall to the precipitation and to atmospheric radon daughters concentration were investigated. It has become clear that when precipitation is small, radon daughters concentration in snowfall is distributed in a wide range, and that the quantity of radon daughters brought to ground surface by snowfall is proportional to precipitation. Washout effect of the snowfall on atmospheric radon daughters was also investigated.

Atmosphere↗
PubMed1983

Species and strain differences in mepirizole-induced duodenal and gastric lesions.

Species and strain differences in mepirizole-induced duodenal and gastric lesions were studied. Mepirizole at 200 mg/kg given orally induced deep duodenal ulcers and gastric erosions in nonfasted Sprague-Dawley, Fisher, Wistar, and Donryu rats at an incidence of over 75%. Mepirizole at 300 mg/kg given orally also induced penetrating duodenal ulcers in nonfasted rabbits at an incidence of 50%. There was little or no damage to the duodenum and stomach in mice and dogs given 200-300 mg/kg of mepirizole orally or subcutaneously. The stomachs of fasted guinea pigs given 200 mg/kg of mepirizole had superficial erosions at a high incidence (93.3%). Mepirizole at 200 mg/kg given intraduodenally significantly reduced the volume of gastric juice but increased the acidity and pepsin activity in both pylorus-ligated and acute fistula rats. In chronic fistula rabbits, however, the agent at 200 mg/kg given orally reduced the volume and acidity, but increased the pepsin activity. The mechanism of duodenal ulceration by mepirizole differs slightly in rats and rabbits.

Animals↗
PubMed1983

Role of luminal alkalinization in repair process of ethanol-induced mucosal damage in rat stomach.

Changes in transmucosal potential difference (PD) and luminal pH after intragastric application of ethanol were simultaneously determined in stomachs of anesthetized rats. When the stomachs were exposed to 5-50% ethanol for 10 min, the PD was abruptly reduced and gradually returned to the basal levels, while the luminal pH gradually increased; these responses were concentration-dependent. The reduction of PD with 10% ethanol rapidly returned to the basal level without any changes in luminal pH. The PD after 50% ethanol gradually returned to the basal level in 3 hr, during which time luminal pH was kept at around 6. In cimetidine plus atropine-treated rats, considerably greater amounts of HCO3- were evident in the perfusate. The surface mucosal cells damaged by 50% ethanol recovered in parallel with the recovery of PD. When the stomach pH was maintained at a low level by an intravenous infusion of histamine or intragastric perfusion of 0.01 N HCl, the PD remained at a reduced level and the mucosal damage was aggravated. The perfusion of 0.01 N NaHCO3 kept the luminal pH at around 8-9, but it did not affect the recovery process of PD after 50% ethanol. These results suggest that application of ethanol induces luminal alkalinization, probably by HCO3- diffusion through the broken barrier, which in turn plays a role in the recovery from damage.

Acid-Base Equilibrium↗
PubMed1983

Effects of an antiulcer drug, sucralfate (a basic aluminum salt of sulfated disaccharide), on experimental gastric lesions and gastric secretion in rats.

The effects of oral sucralfate, a basic aluminum salt of sulfated disaccharide, on various experimental gastric lesions and on gastric secretion were studied in rats. Sucralfate at 300 mg/kg potently inhibited the development of Shay ulcers and indomethacin- and aspirin-induced erosions. The drug at 1000 mg/kg also potently inhibited histamine-induced erosions. Water-immersion stress-induced erosions were inhibited with 1000 mg/kg of the drug, but the degree of inhibition was weaker than that seen in other types of erosion formation. Sucralfate at 1000 mg/kg given twice daily for 14 days significantly accelerated the spontaneous healing of acetic acid-induced ulcers. Sucralfate at over 300 mg/kg tended to increase the volume of gastric juice but had an insignificant effect on acid and pepsin output of pylorus-ligated rats. As a whole, the effects of sucralfate on experimental gastric lesions appear to be much more potent than Maalox, propantheline bromide, and cimetidine. The mechanism of action of sucralfate remains to be determined.

Acetates↗
PubMed1983

Effects of 16,16-dimethyl-PGE2-methyl ester on aspirin- and indomethacin-induced gastric and intestinal lesions in mini pigs.

Aspirin, 100 mg/kg, given only twice at intervals of 16 h to fasted mini pigs induced lesions in the body but had no effect on the antrum and small intestine. Indomethacin, 40 mg/kg, given once daily for 10 consecutive days to non-fasted mini pigs very weakly irritated the pig stomach but induced multiple superficial lesions in the jejunum and ileum. 16,16-Dimethyl-PGE2-methyl ester, 10 micrograms/kg in two divided doses or 20 micrograms/kg in four divided doses for 10 days, markedly inhibited the aspirin- or indomethacin-induced gastric and intestinal lesions in mini pigs, respectively.

16,16-Dimethylprostaglandin E2↗
PubMed1983

Effects of antiulcer agents on healing of mepirizole-induced duodenal ulcers in rats.

Healing processes of duodenal ulcers induced by mepirizole and effects of several drugs on the ulcer healing were studied in rats. Mepirizole-induced duodenal ulcers, except for the perforated ones within 3 days after ulceration, gradually diminished in size and depth by the 15th day. Several ulcers persisted for up to 40 days, but complete healing in all rats occurred by the 60th day after ulceration. Oral cimetidine and YM-11170 (both histamine H2-receptor antagonists), at 200 and 30 mg/kg twice daily for 10 days, respectively, significantly accelerated the healing of duodenal ulcers. Oral Maalox (antacid) at 1,000 mg/kg thrice daily and propantheline (anticholinergic agent) at 30 mg/kg twice daily tended to accelerate the healing of the ulcers. Oral 16,16-dimethyl PGE2, at 0.03 and 0.1 mg/kg twice daily, resulted in a delayed healing of the ulcers. Mepirizole-induced duodenal ulcers appear to be a useful model for the study of ulcer healing and for screening of antiulcer drugs.

Aluminum Hydroxide↗
PubMed1983

Acid back-diffusion and mucosal H+ handling in the rat stomach under normal and stress-induced conditions.

We determined acid back-diffusion and pepsin output simultaneously in vagotomized rats after instillation of HCl into the stomach under normal and stress-induced conditions. With exposure to 6 ml of 100 mM HCl, spontaneous acid back-diffusion increased with the duration of the experiment under both conditions, and the magnitude of the acid back-diffusion was decreased significantly by stress. There was no change in the output of pepsin. While disappearance of luminal acid caused by aspirin or taurocholic acid was not altered by stress, the pepsin output in response to H+ increased significantly in the stressed rats. With exposure to various concentrations of HCl for 3 hr, disappearance of the luminal acid increased linearly with the grade of HCl under both conditions. Except for the concentration of 300 mM, the magnitude of the acid back-diffusion was triple in the normal condition, and the ratio of pepsin output/net flux of H+ was significantly increased by stress. Thus, (1) spontaneous acid back-diffusion decreased with stress, while diffusion induced by chemical barrier breakers remained the same; (2) the action of H+ diffused back into the mucosa did not always parallel the amount of diffusion determined from the loss of H+ in the lumen; (3) intramucosal H+ may be largely dissipated in normal mucosa; and (4) the initiation or aggravation of drug-induced mucosal damages by stress may be related to insufficiency of the H+ dissipating mechanisms.

Animals↗
PubMed1983

Atypical adult T-cell leukemia-lymphoma: diverse clinical manifestations of adult T-cell leukemia-lymphoma.

The diverse clinical manifestations of 10 cases of so-called adult T-cell leukemia-lymphoma (ATL)-related T-cell malignancies are described. These cases were anti-ATLA [antibody to ATL virus (ATLV)-associated antigen (ATLA)] positive, and tumor cells had the inducer/helper T-cell phenotype and expressed ATLA when cultured, indicating that these diseases are the same as typical ATL, even though their clinical diagnoses were different from ATL. Accordingly, they are called atypical ATL. Clinically, they could be divided into two subtypes, smoldering type and lymphoma type. In the smoldering type, the disease usually started with skin lesions and rarely with lung lesions. After a prodromal stage of several years, the disease progressed insidiously to the leukemic stage without additional manifestations. The flower cells characteristic of typical ATL were observed in only a small percentage of peripheral lymphoid cells. In two of the five patients the disease progressed to typical ATL after several years from onset. All five patients are alive with a long survival time, more than 6 yr in four, and had high titers of anti-ATLA, suggesting that anti-ATLA might have some role in regulating the proliferation of ATL cells in vivo. In the lymphoma type, morphological diagnosis was not always specific for discriminating ATL-related from ATL-unrelated T-cell lymphomas. Detection of anti-ATLA in the patient's serum and of ATLA in cultured tumor cells, examination of the sera of members of the patient's family for anti-ATLA, and observation of typical flower cells in the peripheral blood though the patients had neither lymphocytosis nor leukemic changes, seem to be useful for the discrimination, especially in an ATL-nonendemic area. Members of the family of a patient with anti-ATLA positive T-lymphoma in an ATL-nonendemic area were also anti-ATLA positive, indicating that healthy ATLV carriers in an ATL-nonendemic area exist as a family colony. This is responsible for sporadic outbreaks of ATL in an ATL-nonendemic area. In summary, the disease entity of ATL is considered, at present, to be a malignancy of inducer/helper T-cells transformed by ATLV or HTLV (human T-cell leukemia virus). In this sense, diverse clinical manifestations of ATL should be recognized as events of viral oncogenesis and host immune response.

Adult↗
PubMed1983

[Effects of SM powder, a combined herbal preparation for stomach diseases, on gastric secretion and acute gastro-duodenal lesions in rats].

One gram of SM powder consists of 167.8 mg of Coptidis Rhizoma Pulveratum, 250 mg of Cinnamomi Cortex Pulveratus, 67.1 mg of Foeniculi Fractus Pulveratus, 33.6 mg of Caryophylli FLos Pulveratus, 82.1 mg of Zingiberis Rhizoma Pulveratus, 3.4 mg of Zanthoxyli Fructus Pulveratus, and 396 mg of Glycyrrhizae Radix Pulberata. SM powder (2 g/kg, i.d.) significantly inhibited gastric secretion in pylorus-ligated rats and the development of Shay ulcers and indomethacin-induced gastric lesions. The mechanism of the anti-lesion activity of SM powder appears to be due to its antisecretory effect. SM powder also markedly inhibited ethanol- or NaOH-induced gastric lesions at doses (30 or 100 mg/kg) which had little effect on gastric secretion. SM powder appears to have a cytoprotective activity which is unrelated to endogenous prostaglandins. However, SM powder had no effect on water-immersion stress- or aspirin-induced gastric lesions and mepirizole-induced duodenal ulcers. Gentiana Radix Pulverata, used as a reference stomatic, had also an antisecretory effect and anti-lesion activity on Shay ulcers, aspirin-, ethanol- and NaOH-induced gastric lesions. However, it had no effect on water-immersion stress- or indomethacin-induced gastric lesions and mepirizole-induced duodenal ulcers.

Animals↗
PubMed1982

Mepirizole-induced duodenal ulcers in rats and their pathogenesis.

Duodenal ulcers were produced in rats following either an oral or parenteral administration of 200 mg/kg of mepirizole, a nonsteroidal antiinflammatory agent. Deep ulcers, including perforated ones, were induced in the proximal duodenum with an incidence of over 90%. Mortality due to perforation was less than 5%. The agent also induced several erosions in the antrum. Feeding of animals after the ingestion of mepirizole markedly suppressed the development of both duodenal ulcers and gastric erosions. Antacids, anticholinergic agents, a histamine H2-receptor antagonist and 16-DMPGE2 dose-dependently inhibited mepirizole-induced duodenal ulcers. Gastric erosions were also significantly inhibited by antacids and anticholinergic agents but not by a histamine H2-receptor antagonist and 16-DMPGE2. Intraduodenally administered mepirizole dose-dependently inhibited the gastric secretion in pylorus-ligated rats. This ulcer model should be useful for screening antiulcer agents and for the study of pathogenesis of duodenal ulcers and gastric erosions.

Administration, Oral↗
PubMed1982

Effects of the antiulcer drug geranylgeranylacetone on aspirin-induced gastric ulcers in rats.

Antiulcer effects of geranylgeranylacetone (GGA) on aspirin-induced gastric ulcers in rats were studied, comparing them with those of gefarnate. The oral administration of GGA prevented the development of gastric ulcer induced by a single or repeated oral administration (5 consecutive days) of aspirin. The effects of GGA were more potent and more definite than those of gefarnate. The intraduodenal administration of GGA, but not the intragastric administration, also inhibited the ulceration induced by aspirin in pylorus-ligated rats, while the intraduodenal administration of gefarnate did not. GGA prevented the reduction of the H+ concentration and the increment of Na+ concentration in the gastric juice induced by aspirin. In addition, the decrease of hexosamine content in the gastric mucosa induced by aspirin was restored to a normal level by GGA, but not by gefarnate. From these results, it was concluded that the protective actions of GGA on aspirin-induced gastric ulcers might be due to its protection from the weakening of gastric mucosal resistances.

Animals↗
PubMed1982

Effects of CL-1700 and its constituents on acute or chronic gastric lesions and gastric secretion in rats.

Effects of CL-1700 (N-acetyl-L-carnosine aluminum) and its constituents, L-carnosine, N-acetyl-L-carnosine and Al(OH)3 on acute or chronic gastric lesions in intact rats and on gastric secretion in pylorus-ligated rats were studied. CL-1700 at 600 or 1,000 mg/kg p.o markedly inhibited Shay ulcers or indomethacin-induced erosions, but its constituents at the doses contained in CL-1700 did not. Also, CL-1700 at 300 mg/kg i.p. significantly inhibited water-immersion stress-induced erosions, but its constituents did not. CL-1700 at 600 mg/kg i.p. and Al(OH)3 at 143 mg/kg i.p. significantly inhibited Shay ulcers. CL-1700 at 1,000 mg/kg p.o. almost completely inhibited aspirin- or histamine-induced erosions, but both L-carnosine at 639 mg/kg p.o. and N-acetyl-L-carnosine at 817 mg/kg p.o. also markedly inhibited the formation of erosions. CL-1700 at 1,000 mg/kg p.o. increased the volume and raised the pH value, and the agent at 600 mg/kg i.p. reduced the acid output. CL-1700 at 1,000 mg/kg/day p.o. given twice daily for 3 weeks diminished the size of acetic acid ulcers and significantly increased the number of rats with healed ulcers.

Aluminum Hydroxide↗