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Biomedical subjects

A Terano

Publications and source records attributed to A Terano.

At least 181 records · Page 10Linked to original sources
PubMed1988

Prostaglandin E2 output by isolated rat gastric parietal cells and non-parietal epithelial cells.

Prostaglandins have acid antisecretory and cytoprotective effects in gastric mucosa when given exogenously. This study's purpose was to isolate preparations of parietal and non-parietal cells from rat stomachs and to compare prostaglandin output by these cells. Gastric epithelial cells were isolated from rat stomachs using pronase. Cells from different incubation times were collected separately and enriched by discontinuous Percoll gradient. Cell types were identified by hematoxylin and eosin stain, succinic dehydrogenase activity (parietal cells), periodic acid Schiff staining (mucous cells), Bowie staining (chief cells) and electron microscopy. Prostaglandin E2 activity was measured by radio-immunoassay. Parietal cells were purified to over 90% while the non-parietal preparation contained 67% chief cells and over 31% mucous cells. By electron-microscopy, cell integrity was seen to be maintained. The parietal cell enriched fraction contained two and one-half times the amount of prostaglandin E2 that the non-parietal chief cell enriched fraction did, p less than 0.01. These results raise the question as to whether output of PGE2 by parietal cells could play a role in modulating gastric acid secretion directly by parietal cells as well as in protecting the deeper layers of gastric mucosa against damaging agents in-vivo.

Animals↗
PubMed1988

Salicylate effects on a monolayer culture of gastric mucous cells from adult rats.

Aspirin, acetyl salicylic acid, damages gastric mucosal cells. This effect is considered related to its inhibition of prostaglandin synthesis. On the other hand, sodium salicylate has been reported to be cytoprotective against drug damage to gastric mucosa in vivo. One reason for this difference is that salicylic acid, unlike acetyl salicylic acid does not inhibit prostaglandin synthesis by gastric mucosa in vivo. Previous studies on tissue culture cells from our laboratory have required gastric mucosa from fetal rats; this was time consuming and expensive. The purpose of this study was to develop a primary cell culture of adult rat fundic epithelial cells and to test the effect of sodium salicylate on: (1) prostaglandin (PGE2) production, (2) cell viability, (3) reducing cell damage by sodium taurocholate. Gastric epithelial cells were isolated from adult rat stomachs and cultured on collagen gel. Cells reached confluency on day 4 at which stage fibroblasts were rarely seen (less than 1%). Autoradiographic study showed that cultured cells incorporated [3-H] thymidine into nuclei. In histochemical studies, 94% of the cells contained PAS positive granules (mucous cells). Mucous granules were observed in the cytoplasm of the majority of cells by electronmicroscopy. These cells synthesised prostaglandin E2 as determined by radioimmunoassay. Indomethacin 10(-4) M strongly suppressed PGE2 production after 30 minutes while 10(-3) and 10(-4)M sodium salicylate had no effect. Pharmacologic concentrations of 10 mM sodium salicylate had no effect on PGE2 production at 30 minutes and only weakly inhibited production after one hour incubation. Sodium salicylate up to 30 mM had no effect on cell viability, a concentration of 50 mM being necessary to produce significant cell damage. Sodium salicylate 10 mM significantly protected cells against damage induced by 10 mM sodium taurocholate. We conclude: (i) adult rat gastric mucous epithelial cells can be successfully cultured in vitro; (ii) prostaglandin synthesis is inhibited by indomethacin but not by low doses of sodium salicylate; (iii) sodium salicylate does not damage gastric mucosal cells except at very high concentrations; (iv) sodium salicylate protects against damage to cells induced by sodium taurocholate.

Animals↗
PubMed1988

[A case of superficial carcinoma of the esophagus on esophageal varices].

We report a case of superficial esophageal carcinoma in a patient with esophageal varices. Esophagogram revealed a 2 cm large irregular mucosal elevation during work-up for esophageal varices which was acertained on endoscopical examination to be carcinoma. Biopsy material showed moderately differentiated squamous cell carcinoma. Subtotal esophagectomy was performed followed by reconstruction by cervical esophagogastrostomy through the retrosternal route. Few resected cases of esophageal carcinomas accompanied by esophageal varices have been reported because 1) early radiographic abnormalities of small superficial esophageal carcinomas can be overlooked in the case of large varices and 2) the number of operable cases is limited because of associated liver cirrhosis.

Biopsy↗
PubMed1987

Arachidonic acid stimulation of mucus production by rat gastric cultured cells.

The effect of arachidonic acid (AA) on mucus production (synthesis and secretion) by rat gastric monolayer-cultured cells was investigated. For the study of mucus synthesis, the rate of incorporation of [3H]glucosamine into the cultured cells was measured. The rate of release of glycoprotein into the culture media from the cells, which were incubated in the medium containing [3H]glucosamine for 24 hr in advance, was determined for the study of mucus secretion. Prostaglandins in the medium were measured by radioimmunoassay. AA (10(-4) M) significantly increased mucus synthesis and secretion by the cultured cells (P less than 0.01). PG (E2 and I2) synthesis by the cultured cells was significantly enhanced by AA (10(-4) M) (P less than 0.05). An addition of indomethacin to the culture medium abolished this effect of AA. These results suggested that gastric mucus production was enhanced by AA in vitro and that this effect may be mediated by endogenous PG production.

Animals↗
PubMed1987

Arachidonic acid does not protect against sodium taurocholate damage to rat gastric epithelial cell cultures.

Arachidonic acid is cytoprotective against ethanol damage in vivo. Stimulation of production of endogenous prostaglandin has been postulated as a mechanism of this protection. The current study assessed the ability of arachidonic acid to protect gastric mucosal cells directly and the effect of arachidonic acid on prostaglandin production. To determine cytoprotection, sodium taurocholate was used as a damaging agent and cell viability was assayed by 51Cr release in vitro. By the dose response curve, 5 mM sodium taurocholate was chosen for the protective study. Cells were preincubated with arachidonic acid (0.1-10 micrograms/ml) and then incubated with 5 mM sodium taurocholate. The synthetic activity of prostaglandins by cultured cells was assessed using 14C arachidonic acid prelabeled cells. Media content of prostaglandin E2 was assayed by radioimmunoassay. Cell viability was assayed by 51Cr release. Our results showed that arachidonic acid did not significantly protect cultured gastric cells against sodium taurocholate damage, while larger doses of arachidonic acid produced cell damage. Furthermore, cultured gastric cells produced mainly prostaglandin E2 and prostaglandin I2 and arachidonic acid stimulated prostaglandin E2 production dose-dependently (p less than 0.01). In conclusion, arachidonic acid does not directly protect gastric mucosal cells in vitro. In vivo protection by arachidonic acid must be based on indirect factors such as preservation of microvasculature.

Animals↗
PubMed1987

Prostaglandin protects against taurocholate-induced damage to rat gastric mucosal cell culture.

Prostaglandins protect gastric mucosa against noxious agents, but it is unknown whether this protection includes a direct action on the cells themselves, this action is limited to damaging agents that inhibit prostaglandin synthesis, or cellular cyclic adenosine monophosphate is the mediator. The present study tested these questions in cultured gastric mucous epithelial cells. The effect of 16,16-dimethyl prostaglandin E2 on cellular cyclic adenosine monophosphate level and the effect of 16,16-dimethyl prostaglandin E2, dibutyryl cyclic adenosine monophosphate, and isobutyl methyl xanthine on taurocholate-induced damage to cultured rat gastric mucosal cells was determined. As parameters of cell damage, the trypan blue dye exclusion test and 51Cr-release were employed. Taurocholate significantly increased 51Cr-release in a dose-dependent manner and decreased the number of viable cells. 16,16-Dimethyl prostaglandin E2 (1.0 microM) diminished the cell damage caused by 10 mM taurocholate (p less than 0.01) and increased cyclic adenosine monophosphate levels. Prostaglandin F2 alpha but not prostaglandin I2 was also cytoprotective. Addition of dibutyryl cyclic adenosine monophosphate (1.0 mM) and isobutyl methyl xanthine while significantly increasing cyclic adenosine monophosphate levels did not significantly reduce taurocholate-induced cell damage. Thus, in vitro 16,16-dimethyl prostaglandin E2 directly protects gastric mucous cells against taurocholate-induced injury, direct prostaglandin cytoprotection is not limited to damaging agents that inhibit prostaglandin synthesis, and cyclic adenosine monophosphate levels do not correlate with gastric mucosal cell damage and may not be involved in the direct protective effect of prostaglandins.

16,16-Dimethylprostaglandin E2↗
PubMed1987

Mucin-hypersecreting carcinoma of the pancreas.

Five cases of prominent, diffuse dilatation of the main pancreatic duct caused by mucin-hypersecreting carcinoma are reported. Adenocarcinoma was noted mainly within one markedly dilated main pancreatic duct. On endoscopic retrograde pancreatograms, dilated main pancreatic ducts with amorphous or well-defined filling defects resulting from mucin (five patients) or tumor (one patient) were noted. The proximal portion of the main pancreatic duct alone was delineated in three cases because of reflux of contrast material as a result of the presence of excessive mucin and a patulous orifice of the papilla of Vater (major duodenal papilla). Diffuse dilatation of the main pancreatic duct was demonstrated or suggested on computed tomographic (CT) and ultrasound scans. Four patients who underwent operations are alive and free from carcinoma (mean, 50 months after diagnosis). Whenever prominent, diffuse dilatation of the main pancreatic duct is encountered on CT or ultrasound scans, endoscopic retrograde pancreatography is mandatory to permit confirmation or ruling out of mucin-hypersecreting carcinoma of the pancreas.

Adenocarcinoma↗
PubMed1987

Oxygen metabolite-induced cytotoxicity to cultured rat gastric mucosal cells.

Reactive oxygen metabolites have been reported to be responsible for the pathogenesis of ischemia-induced gastric mucosal lesions. We have investigated the possible protective effect of specific enzymes and oxygen radical scavenging agents on oxygen metabolite-induced injury to cultured gastric mucosal cells. Oxygen-reactive metabolites were generated by 1 mM xanthine and 10-100 mU/ml xanthine oxidase. Cytotoxicity was quantified by measuring 51Cr release from prelabeled cells. Xanthine oxidase caused a dose-dependent increase of 51Cr release in the presence of 1 mM xanthine. Catalase (an enzyme that reduces hydrogen peroxide) diminished xanthine-xanthine oxidase-induced 51Cr release in a dose-dependent manner. Superoxide dismutase (a scavenger of superoxide radical) failed to affect the amounts of 51Cr release induced by xanthine plus xanthine oxidase. Pretreatment with diethyl maleate, which depletes intracellular glutathione, potentiated oxygen radical-mediated 51Cr release dose dependently. The presence of ferrous ion or ethylenediaminetetraacetic acid-chelated iron, which promote the formation of hydroxyl radical, did not alter xanthine-xanthine oxidase-induced cellular injury. Furthermore, agents that inactivate hydroxyl radical also failed to protect the cells from oxygen metabolite-induced injury. We conclude that in vitro oxygen metabolites, extracellularly generated, have a direct toxic effect on gastric mucosal cells; hydrogen peroxide is a major mediator of oxygen metabolite-induced gastric cell injury; the oxygen-derived superoxide and hydroxyl radicals are less toxic to gastric mucosal cells than hydrogen peroxide; and intracellular glutathione, which detoxifies hydrogen peroxide, may be involved in antioxidant defense mechanisms.

Animals↗
PubMed1987

Prominent collateral vein in portal hypertension mimicking liver tumours: a pitfall in computed tomography.

Computed tomography (CT) was performed on four patients with a prominent porto-systemic collateral vein, including three with an enlarged para-umbilical vein. We have observed a pitfall in non-contrast CT scans of patients with portal hypertension, in which a prominent collateral vein may mimic a liver tumour. Dynamic CT as well as magnetic resonance imaging is of great value in such cases.

Diagnosis, Differential↗
PubMed1986

Prostaglandin production in cultured gastric mucosal cells: role of cAMP on its modulation.

The effect of cAMP on prostaglandin production may depend on cell types. To clarify the relationship between PG and cAMP, we examined arachidonate's effects on PG synthesis and intracellular cAMP accumulation in monolayers of rat gastric mucosal cells. These cells produced PGE2, PGI2 and thromboxaneA2 (TXA2) in amounts of 316 +/- 18, 100 +/- 7 and 30 +/- 5 pg per 10(5) cells in 10 min, respectively, in response to 10 microM arachidonic acid (AA). The production of these PG, however, leveled off subsequently. Cells initially exposed to AA responded poorly to a subsequent stimulation by AA. AA simultaneously stimulated intracellular cAMP accumulation; this stimulatory effect on cAMP production was abolished by the pretreatment with indomethacin. Nevertheless, the pretreatments with dibutyryl cAMP (0.1-5 mM) did not alter the amount of subsequent AA-induced PGE2 production. Furthermore, the preincubation with 1mM isobutyl methyl xanthine also failed to affect PGE2 synthesis, while it increased intracellular cAMP accumulation. Our studies suggest AA stimulates intracellular cAMP formation in cultured gastric mucosal cells, linked with conversion of AA to cyclooxygenase metabolites, AA-induced PG production is limited in these cells, and it seems, however, unlikely that intracellular cAMP modulates AA metabolism to PG.

Animals↗
PubMed1986

Geranylgeranylacetone, a novel anti-ulcer drug, stimulates mucus synthesis and secretion in rat gastric cultured cells.

Aim of this study was to investigate the effect of geranylgeranylacetone (GGA) on mucus synthesis and secretion in rat gastric cultured cells, and their relationship to prostaglandin (PG) synthesis. Rate of mucus synthesis was estimated by incorporation of 3H-glucosamine into the cultured cells. Release of 3H-glucosamine from the cells, which were preincubated in the medium containing the radioactive isotope, into the culture media was measured for the evaluation of mucus secretion. PG production by the cultured cells was measured by radioimmunoassay. GGA increased glycoprotein synthesis in a dose-dependent manner (p less than 0.01). Secretion of mucus from cultured cells was also significantly enhanced by GGA. GGA did not significantly increase PG (E2 and I2) production. These results indicate that GGA has the ability to stimulate mucus production by the gastric epithelial cells, and this action may play an important role in protective effect of GGA. It is, however, unlikely that this effect of GGA is mediated by endogenous PGs.

Animals↗
PubMed1986

Protective action of tetraprenylacetone against ethanol-induced damage in rat gastric mucosa.

The purpose of this study was to investigate the morphological and physiological effects of tetraprenylacetone (TPA) on ethanol(ET)-induced injury in rat gastric mucosa. Fasted rats received orally the following agents; a) vehicle (VH); b) 50, 100, or 200 mg/kg of TPA; c) indomethacin (IDM, 5 mg/kg), 30 min prior to TPA (200 mg/kg). Thirty minutes later, 1 ml of absolute ET was administered into the rat stomach. The gastric mucosa was assessed at 60 min after administration of ET. The ulcer index was significantly decreased by TPA in a dose-related fashion when compared with controls. Histological studies also showed significant reduction of ET-induced mucosal damage by TPA. A scanning electron microscopic study revealed that, when TPA was administered, surface epithelial cells of fundic mucosa were protected against ET-induced injury. The decrease of potential difference induced by ET was diminished by TPA (p less than 0.01). Addition of IDM significantly reduced the effect of TPA. This indicates that TPA has a protective effect on rat gastric mucosa against ET-induced injury. The data also suggested that endogenous prostaglandins may be partially involved in this effect of TPA.

Animals↗
PubMed1986

Effect of cimetidine on indomethacin-induced damage in cultured rat gastric mucosal cells; comparison with prostaglandin.

Whether cimetidine protects gastric mucosal cells independently of its antisecretory effect has been controversial. Some investigators postulate that, on the contrary, cimetidine decreases the integrity of gastric mucosa. Furthermore, whether cimetidine influences gastric prostaglandin (PG) synthesis is debated. Therefore, we investigated and compared with 16,16-dimethyl-PGE2 (dmPGE2) whether cimetidine protects cultured rat gastric mucosal cells from indomethacin, and tested whether cimetidine affects gastric PG production by these cells. Cell damage was assessed by chromium 51-release assay. Concentrations of indomethacin greater than 1 mmol/L caused cell damage and increased 51Cr release in a dose-dependent and time-dependent fashion. dmPGE2 significantly reduced indomethacin-induced increase of 51Cr release, whereas cimetidine at both nonantisecretory and antisecretory doses did not alter 51Cr release caused by indomethacin. The cultured cells released PGE2 and PGI2 in amounts of 215 +/-18 and 56 +/- 3 (mean +/- SEM) pg/10(5) cells in 1 hour, respectively. Nondamaging concentrations of indomethacin caused a dose-dependent inhibition of PG release from cultured cells with 50% inhibitory concentration at a dose of 10(-6) to 10(-7) mol/L. Cimetidine did not alter gastric PG production. In summary, exogenous PG protected gastric mucosal cells from indomethacin in vitro, but cimetidine did not. In conclusion, cimetidine, which fails to affect gastric PG production, does not directly influence the integrity of gastric mucosal cells.

Animals↗