This experiment was performed to evaluate the morphological responses of the gastric parietal cells of mouse inoculated with Ehrlich carcinoma cells, following administration of Bacillus Calmette -Guerin (BCG) or acriflavine -guanosine composition (AG60, Taerim Pharm. Co. Seoul, Korea). In the experimental groups, each mouse was inoculated with 1 X 10(7) Ehrlich carcinoma cells subcutaneously in the inguinal area. From next day, 0.2 ml of saline, BCG (0.03 X 10(8) ~0.32 X 10(8) CFU) or AG60 (30 mg/kg) was injected subcutaneously to the animals every other day. Animals were sacrificed on the 14th day from the first injection. Pieces of the tissue were taken from the stomach, prefixed with 2.5% glutaraldehyde -1.5% paraformaldehyde, followed by post -fixation with 1% osmium tetroxide. The ultrathin sections stained with uranyl acetate and lead citrate were observed with a JEM 100CX -II electron microscope. In the experimental control, the BCG and the AG60 treated groups, most parietal cells showed reduced lumenal spaces of the intracellular canaliculi, since microvilli of intracellular canaliculi were very irregularly shaped and crowed with each other. And in the BCG and the AG60 treated mice, myelin figures, lysosomes and multivesicular bodies in the parietal cells were observed more frequently than in those of the experimental control ones. In the BCG treated rats, membranes of the tubulovesicles of the parietal cells were disintegrated, but the similar changes were not observed in the AG60 treated mice,. Above results suggest that the BCG treated animals inoculated with Ehrlich carcinoma cells might suffer from reduced acid secretion of the parietal cell, since the disintegration of the tubulovesicular membranes in the parietal cells are occurred following injections. Whereas AG60 dose not affect remakably defect on the parietal cells.
Acriflavine ; Animals ; Bacillus ; Citric Acid ; Crows ; Gastric Mucosa ; Glutaral ; Lysosomes ; Membranes ; Mice* ; Microvilli ; Multivesicular Bodies ; Mycobacterium bovis* ; Myelin Sheath ; Osmium Tetroxide ; Parietal Cells, Gastric* ; Rabeprazole ; Rats ; Seoul ; Stomach

This experiment was performed to evaluate the morphological responses of 5-fluorouracil or mitomycin C on the gastric parietal cells of mouse. 5 -fluorouracil (30 mg/kg) or mitomycin C (400 micro gram/kg) were injected subcutaneously every other day, and the animals were sacrificed at 4th day and 7th day following the first injection. Pieces of the tissue were taken from the stomach, prefixed with 2.5% glutaraldehyde -1.5% paraformaldehyde, followed by post-fixation with 1% osmium tetroxide. The ultrathin sections were stained with uranyl acetate and lead citrate. In both of the 5-fluorouracil or the mitomycin C treated groups, most parietal cells showed severely reduced luminal spaces of the intracellular canaliculi, since microvilli of intracellular canaliculi were very irregular shaped and nearly contacted with each other, and the cytoplasmic tubulovesicular membranes were disintegrated and indistinct. The changes in the 5-fluorouracil treated group were more indistinct than in those of the mitomycin C treated group. In the 5-fluorouracil treated group, balooning of the cytoplasm, focal cytolysis, myelin figures, lysosomes and multivesicular bodies in the parietal cells were observed more frequently than in those of the mitomycin C treated group. Above results suggest that the 5-fluorouracil or mitomycin C treated animals might suffer from reduced acid secretion of the parietal cell, since the collapsed lumen of the intracellular canaliculi, the disintegration of the tubulovesicular membranes, and the reduction of cell organelles in the parietal cells are occurred within a few days following injections. 5-fluorouracil was proved more harmful on the parietal cell than mitomycin C does.
Animals ; Citric Acid ; Cytoplasm ; Fluorouracil* ; Gastric Mucosa ; Glutaral ; Lysosomes ; Membranes ; Mice* ; Microvilli ; Mitomycin* ; Multivesicular Bodies ; Myelin Sheath ; Organelles ; Osmium Tetroxide ; Parietal Cells, Gastric* ; Phenobarbital ; Rabeprazole ; Stomach

Proton-pump inhibitors (PPI) have important roles in the management of acid-related disorders, especially gastro-esophageal reflux disease and peptic ulcer disease. They are considered safe, but some side effects, such as oxyntic cell hyperplasia, glandular cysts, hypergastrinemia and fundic gland polyps, are also reported. Long-term PPI administration in Helicobacter pylori (H. pylori) positive subjects promotes a shift from antral to corpus-predominant gastritis. The shift leads to corpus atrophy eventually that is known predisposing factor of gastric adenocarcinoma. It is recommended that patients being considered for long-term PPI therapy should be tested for H. pylori infection. And if present, H. pylori eradication should be preceded to PPI administration. Also, long-term PPI administration can cause enterochromaffin-like cell hyperplasia. Although the underlying mechanism and pathogenesis are not yet fully understood, it is possible that long-term PPI administration can promote the development of gastric carcinoid tumor. Therefore, to minimize the side effects, it should be used in adequate dose for a precise duration.
Adenocarcinoma ; Atrophy ; Carbamates ; Carcinoid Tumor ; Enterochromaffin-like Cells ; Gastritis ; Gastritis, Atrophic ; Gastroesophageal Reflux ; Helicobacter pylori ; Humans ; Hyperplasia ; Organometallic Compounds ; Parietal Cells, Gastric ; Peptic Ulcer ; Polyps

Potassium (K+) balance is achieved by the control of urinary K+ excretion and by the control of K+ absorption from the digestive tract. It has been established that chronic potassium depletion is associated with a remarkable hypertrophy of the collecting duct of the kidney. But, there is no morphological studies regarding the stomach and distal colon during the chronic changes of potassium diet. Electron microscopy was performed to observe the morphological alterations of the stomach and distal colon in response to chronic changes of potassium diet in rat. Electron microscopy of normal parietal cells revealed the presences of many mitochondia, tubulovesicles, and short basal cytoplasmic processes and microvilli in the intracellular canaliculi. In potasium-depleted parietal cells, mito-chondria were increased in size and number, and tubulovesicles almost disappeared, and microvilli in the intracellular canaliculi were increased in number and length, and short basal cytoplasmic processes were also increased in size and number. Parietal cells of potassium-loading after restriction were found to be almost normal. Two types of surface columnar epithelial cells were present in normal distal colon. Type I cells had many mitochondria and abundant coated vesicles in the supranuclear region. Type II cells had moderate amount of mitochondria and relatively fewer coated vesicles. In comparison with normal, potasium-depleted surface columnar epithelial cells had more abundant and larger mitochondria and more numerous and longer (1.4~1.6 times than normal) microvilli. Surface columnar epithelial cells of potassium-loading after restriction were recovered almost to normal. These results suggest that gastric parietal cells and surface columnar epithelial cells of distal colon adapt through morphological changes to preserve potassium balance during chronic changes of potassium diet.
Absorption ; Animals ; Coated Vesicles ; Colon* ; Cytoplasm ; Diet ; Epithelial Cells* ; Gastrointestinal Tract ; Hypertrophy ; Kidney ; Microscopy, Electron ; Microvilli ; Mitochondria ; Parietal Cells, Gastric ; Potassium ; Potassium, Dietary* ; Rabeprazole* ; Rats ; Stomach

AIMTo demonstrate the protective effect of nitric oxide (NO) on gastric mucosa and its relationship to the acid secretion of parietal cells under stress in rats.

METHODSWater immersion-restraint stress (WRS) model in SD rats was performed. The gastric mucosal ulcer index (UI), NO contents in gastric mucosa and H+, K(+) -ATPase activity of parietal cells were measured. The effects of N(G)-nitro-L-arginine methyl ester(L-NAME) and L-arginine (L-Arg) on the H+, K(+)-ATPase activity of parietal cells and stress-induced gastric mucosal lesion were observed.

RESULTSL-NAME pretreatment decreased NO contents in gastric mucosa, activated H+, K(+) -ATPase activity of parietal cells and aggravated gastric mucosal lesion, whereas L-Arg pretreatment increased NO contents, inhibited H+, K(+) -ATPase activity and significantly ameliorated stress-induced gastric mucosal lesion.

CONCLUSIONEndogenous nitric oxide plays an important role in protecting gastric mucosa from stress-induced lesion by inhibiting H+, K(+) -ATPase activity of parietal cells.

Animals ; Arginine ; metabolism ; Gastric Acid ; secretion ; Gastric Mucosa ; metabolism ; H(+)-K(+)-Exchanging ATPase ; metabolism ; Male ; Nitric Oxide ; metabolism ; Nitric Oxide Synthase ; metabolism ; Oxidative Stress ; Parietal Cells, Gastric ; metabolism ; Rats ; Rats, Sprague-Dawley ; Stomach Ulcer ; metabolism ; pathology ; Stress, Physiological

Organ specific autoimmune diseases may occur in the same individual. Type III polyglandular autoimmune disease is defined by the occurrence in the same individual of two or more of the following: autoimmune thyroid disease, pernicious anemia, insulin dependent diabetes, and other organ specific autoimmune diseases not falling into class I or class II categories. A 16-year-old girl developed pernicious anemia during the treatment of Graves' disease. She was diagnosed with Graves' disease 5 years ago and had received methimazole 20 mg/day, but the medication was not well tolerated. Bone marrow findings were compatible with pernicious anemia as macrocytic normochromic red blood cell (RBC) and increased megakaryocyte. The serum value of vitamin B12 was low, and the serum titer of antibody to gastric parietal cell was high. After diagnosis of pernicious anemia, she had treatment by monthly intramuscular vitamin B12 and methimazole (20 mg/day). The values of hemoglobin and RBC indices as well as thyroid function were normalized after 2 months. Vitamin B12 therapy was maintained for 1 year with normal RBC indices. At present, she dose not receive treatment with vitamin B12 but she does receive methimazole treatment. We report a case of treatment of pernicious anemia in a 16 year-old girl during treatment for Graves disease.
Adolescent ; Anemia, Pernicious ; Autoimmune Diseases ; Bone Marrow ; Child ; Erythrocytes ; Graves Disease ; Hemoglobins ; Humans ; Insulin ; Megakaryocytes ; Methimazole ; Parietal Cells, Gastric ; Thyroid Diseases ; Thyroid Gland ; Vitamin B 12

Organ specific autoimmune diseases may occur in the same individual. Type III polyglandular autoimmune disease is defined by the occurrence in the same individual of two or more of the following: autoimmune thyroid disease, pernicious anemia, insulin dependent diabetes, and other organ specific autoimmune diseases not falling into class I or class II categories. A 16-year-old girl developed pernicious anemia during the treatment of Graves' disease. She was diagnosed with Graves' disease 5 years ago and had received methimazole 20 mg/day, but the medication was not well tolerated. Bone marrow findings were compatible with pernicious anemia as macrocytic normochromic red blood cell (RBC) and increased megakaryocyte. The serum value of vitamin B12 was low, and the serum titer of antibody to gastric parietal cell was high. After diagnosis of pernicious anemia, she had treatment by monthly intramuscular vitamin B12 and methimazole (20 mg/day). The values of hemoglobin and RBC indices as well as thyroid function were normalized after 2 months. Vitamin B12 therapy was maintained for 1 year with normal RBC indices. At present, she dose not receive treatment with vitamin B12 but she does receive methimazole treatment. We report a case of treatment of pernicious anemia in a 16 year-old girl during treatment for Graves disease.
Adolescent ; Anemia, Pernicious ; Autoimmune Diseases ; Bone Marrow ; Child ; Erythrocytes ; Graves Disease ; Hemoglobins ; Humans ; Insulin ; Megakaryocytes ; Methimazole ; Parietal Cells, Gastric ; Thyroid Diseases ; Thyroid Gland ; Vitamin B 12

To date, most of data regarding H/K-ATPase have been derived from alterations of gene expression or enzymatic activity in kidney. But potassium balance is achieved by the control of urinary K+ excretion and by the control of K+ absorption from the digestive tract. The digestive system is also expected to participate substantively in the regulation of systemic K+ homeostasis during chronic hypokalemia. This study was performed to analyze the expression and distribution of the gastric H/K-ATPase alpha subunit mRNA and protein in rats of chronic changes of potassium diet using Northern blot analysis and immunohistochemistry. Northern blot analysis demonstrate that gastric H/K- ATPase alpha subunit mRNA was abundantly expressed in normal rat stomach not in distal colon. In experimental groups, gastric H/K-ATPase alpha subunit mRNA was also abundantly expressed, but there was no significant differences among all groups. By immunohistochemistry, immunoreactivity of gastric H/K-ATPase alpha subunit was detected in the parietal cells. Reaction products were diffusely localized throughout the cytoplasm. Most of these immunoreactive cells were located in the gastric gland between the neck and base portion of the body, but a few cells in the base or gastric pits. All groups exhibited comparable cellular patterns of labeling and signal intensity. These results suggest that gastric H/K-ATPase alpha subunit does not significantly contribute to potassium conservation during chronic changes of potassium diet in spite of abundant expression.
Absorption ; Adenosine Triphosphatases ; Animals ; Blotting, Northern ; Colon ; Cytoplasm ; Diet ; Digestive System ; Gastric Mucosa ; Gastrointestinal Tract ; Gene Expression ; Homeostasis ; Hypokalemia* ; Immunohistochemistry ; Kidney ; Neck ; Parietal Cells, Gastric ; Potassium ; Rabeprazole ; Rats ; RNA, Messenger ; Stomach

OBJECTIVETo study the regulative action of mica monomer powder preparation on the chief and parietal cells as well as G and D cells in the gastric mucosa of the experimental atrophic gastritis (CAG) rats.

METHODSIntervention therapy was given to the experimental CAG rats at three different doses of mica monomer powder preparation to evaluate the changes of chief and parietal cells as well as G and D cells in the gastric mucosa and the histopathological changes of gastric mucosa.

RESULTSMica monomer powder preparation at three different doses could increase the amount of chief and parietal cells as well as G and D cells in gastric mucosa of the experimental CAG rats and alleviate and control the inflammation of gastric mucosa and the atrophy of gastric mucosa glands. Especially, better effects were shown in the mid and high dose groups.

CONCLUSIONMica has the pharmacological action of protecting the gastric mucosa, enhancing blood flow of the gastric mucosa, and consequently improving the inflammatory responses of the gastric mucosa. One of the mechanisms is associated with promoting the secretion of gastric acid and gastric pepsin and regulating the neuroendocrine mechanism including gut hormone secretion (gastrin and somatostatin) by increasing the number of chief and parietal cells as well as G and D cells.

Aluminum Silicates ; pharmacology ; Animals ; Cell Count ; Chief Cells, Gastric ; drug effects ; pathology ; Chronic Disease ; Gastric Mucosa ; drug effects ; pathology ; Gastrin-Secreting Cells ; drug effects ; pathology ; Gastritis, Atrophic ; pathology ; Inflammation ; Parietal Cells, Gastric ; drug effects ; pathology ; Powders ; Rats ; Rats, Sprague-Dawley ; Somatostatin-Secreting Cells ; drug effects ; pathology

OBJECTIVETo observe the effect of selective cyclooxygenase-2 (COX-2) inhibitor on the healing of experimental gastric ulcer in rats and explore its mechanisms in light of gastric acid secretion.

METHODSGastric ulcers were induced in rats by an application of acetic acid to the serosal surface of the anterior gastric body. The effects of selective COX-2 inhibitor, celecoxib, on the healing of gastric ulcer, the total acidity of gastric juice, the expressions of H+, K+-ATPase mRNA and protein, and the ultrastructure of the parietal cell were observed in comparison with the effects of normal saline.

RESULTSNine days after ulcer induction, the ulcer area was 11.9-/+3.1 mm square and 19.7-/+3.8 mm square in rats with normal saline and celecoxib treatments, respectively (P<0.01). The total acidity of gastric juice and the expressions of H+, K+-ATPase mRNA and protein in celecoxib group were significantly higher than that in normal saline group at both 6 and 9 days after ulcer induction, but no significant difference was found between the two groups in the amount of secretary canaliculus and microvillus.

CONCLUSIONSelective COX-2 inhibitor can significantly delay the healing of experimental gastric ulcer in rats, the mechanism of which might be associated with enhanced digestive action of gastric acid on the new granulation tissue at the ulcer base as a result of celecoxib-stimulated gastric acid secretion of the parietal cells.

Animals ; Celecoxib ; Cyclooxygenase 2 Inhibitors ; pharmacology ; therapeutic use ; Gastric Acid ; secretion ; Gene Expression Regulation, Enzymologic ; drug effects ; H(+)-K(+)-Exchanging ATPase ; genetics ; metabolism ; Hydrogen-Ion Concentration ; Male ; Microvilli ; drug effects ; pathology ; Parietal Cells, Gastric ; drug effects ; ultrastructure ; Pyrazoles ; pharmacology ; therapeutic use ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Wistar ; Stomach Ulcer ; drug therapy ; metabolism ; pathology ; Sulfonamides ; pharmacology ; therapeutic use