Ghrelin plasma levels, gastric ghrelin cell density and bone mineral density in women with rheumatoid arthritis

Generalized bone loss can be considered an extra-articular manifestation of rheumatoid arthritis (RA) that may lead to the occurrence of fractures, resulting in decreased quality of life and increased healthcare costs. The peptide ghrelin has demonstrated to positively affect osteoblasts in vitro and has anti-inflammatory actions, but the studies that correlate ghrelin plasma levels and RA have contradictory results. We aimed to evaluate the correlation between total ghrelin plasma levels, density of ghrelin-immunoreactive cells in the gastric mucosa, and bone mineral density (BMD) in twenty adult women with established RA with 6 months or more of symptoms (mean age of 52.70±11.40 years). Patients with RA presented higher ghrelin-immunoreactive cells density in gastric mucosa (P=0.008) compared with healthy females. There was a positive relationship between femoral neck BMD and gastric ghrelin cell density (P=0.007). However, these same patients presented a negative correlation between plasma ghrelin levels and total femoral BMD (P=0.03). The present results indicate that ghrelin may be involved in bone metabolism of patients with RA. However, the higher density of ghrelin-producing cells in the gastric mucosa of these patients does not seem to induce a corresponding elevation in the plasma levels of this peptide.

Association between vitamin B12 level and anti-parietal cells and anti-intrinsic factor antibodies among adult Jordanian patients with Helicobacter pylori infection

OBJECTIVE: Evaluate the association of Helicobacter pylori infection with anti-parietal cell antibodies (APCA) and anti-intrinsic factor antibodies (AIFA) and their impact on vitamin B12 serum level. PATIENTS AND METHODS: One hundred patients (M/F: 43/57; age 46.5 ± 17.5 years) who underwent upper gastrointestinal endoscopy at King Abdullah University Hospital, Irbid, Jordan were enrolled in the study. The patients were grouped as H. pylori-infected (n = 81) or H. pylori negative (n = 19) by histopathological examination. Fasting serum vitamin B12 levels, antiparietal cell antibodies and anti-intrinsic factor antibodies for patients and controls were determined. RESULTS: Anti-parietal cell antibodies and anti-intrinsic factor antibodies were positive in 9.9% and 18.5% of H. pylori-positive patients respectively. None of the H. pylori negative subjects had anti-parietal cell antibodies or anti-intrinsic factor antibodies. Serum vitamin B12 level was lower in the H. pylori-infected patients (275 ± 70.4 pg/mL) than in controls (322.9 ± 60.7 pg/mL; p 0.05). H. pylori was positive in 94% of the low-vitamin B12 group compared with 64.6% of the normal-vitamin B12 group (p 0.5). CONCLUSION: Patients with H. pylori infection are more likely to have anti-parietal cell antibodies and anti-intrinsic factor antibodies. There was an association between H. pylori infection and lower vitamin B12 levels. H. pylori infection might be a significant factor in the pathogenesis of autoimmune gastritis.

A Multicenter Retrospective Analysis of the Clinical Features of Pernicious Anemia in a Korean Population

To determine the approximate incidence and clinical features of pernicious anemia in a Korean population, we retrospectively analyzed clinical data for patients with pernicious anemia who were diagnosed between 1995 and 2010 at five hospitals in Chungnam province. Ninety-seven patients were enrolled, who accounted for 24% of patients with vitamin B12 deficiency anemia. The approximate annual incidence of pernicious anemia was 0.3 per 100,000. The median age was 66 (range, 32-98) yr, and the male/female ratio was 1.25. Anemia-associated discomfort was the most common symptom (79.4%), followed by gastrointestinal and neurological symptoms (78.4% and 38.1%, respectively). Pancytopenia was found in 36 patients (37.1%), and autoimmune disorders were found in 15 patients (15.5%). Antibody to intrinsic factor was detected in 62 (77.5%) of 80 patients examined, and antibody to parietal cells was detected in 35 (43.2%) of 81 patients examined. Of the 34 patients who underwent tests for Helicobacter pylori, 7 (12.5%) were positive. The anemia-associated and gastrointestinal symptoms resolved completely in all patients after intramuscular injection of cobalamin, whereas neurological symptoms remained in some. In conclusion, pernicious anemia is less frequent in Koreans than in Western populations; however, the clinical features of this disorder in Koreans do not differ from those of Western cases.

Neurological disorders associated with glutamic acid decarboxylase antibodies: a Brazilian series / Distúrbios neurológicos associadas a anticorpos anti-GAD (descarboxilase do ácido glutâmico): uma série de casos brasileira

Neurological disorders associated with glutamic acid decarboxylase (GAD) antibodies are rare pleomorphic diseases of uncertain cause, of which stiff-person syndrome (SPS) is the best-known. Here, we described nine consecutive cases of neurological disorders associated with anti-GAD, including nine patients with SPS and three cases with cerebellar ataxia. Additionally, four had hypothyroidism, three epilepsy, two diabetes mellitus and two axial myoclonus.

Distúrbios neurológicos associados com anticorpos anti-GAD são doenças pleomórficas, raras, de causa incerta, das quais a rigidez muscular espasmódica (SPR) é a mais conhecida. Neste estudo, descrevemos nove casos consecutivos de distúrbios neurológicos associados com a presença de anticorpos anti-GAD, incluindo nove pacientes com SPR e três casos com ataxia cerebelar. Adicionalmente, foram encontrados quatro casos com hipotireoidismo, três com epilepsia, dois com diabetes mellitus e dois casos com mioclonia axial.

The Treatment of Pernicious Anemia in Children with Graves' Disease

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.

The Treatment of Pernicious Anemia in Children with Graves' Disease

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.

The morphological effects of asthma, as well as conventional and alternative asthma therapies on parietal and chief cells in the stomach of BALB/c Mice / Los efectos morfológicos del asma, así como de las terapias convencionales y alternativas del asma sobre las células parietales y principales en el estómago de ratones Balb/c

Scientific literature, although limited in this area, supports the hypothesis that asthma, by means of selective leukocyte trafficking between the various mucosal and glandular sites of the body, can have the same pathophysiological effects on the stomach as the airways. This study aimed to determine if asthma, in the absence and presence of various asthma therapies (Hydrocortisone and Modul8TM), imparted any morphological alteration on the stomach parietal and chief cells. The BALB/c murine asthmatic mouse model was the model of choice in this study. The asthma induction protocol as well as the asthma therapies were proved to be effective with the aid of bronchial lavage fluid leukocyte quantification. Fundic and pyloric biopsies were extracted at termination and assessed by means of transmission electron, scanning electron and light microscopy. The extracted fundic and pyloric biopsies revealed asthma alone induced parietal cell hypertrophy (increase in parietal cell size P < 0.000100 in both stomach regions) and chief cell hyper functioning. The use of Hydrocortisone and Modul8TM, as a therapy to correct the perceived gastric alterations were dismal; only in the case of fundic parietal cells were both treatments able to compensate for the hypertrophic effect caused by asthma, while in the pylorus parietal cell asthma- induced hypertrophy was only compensated for by Modul8TM.

La literatura científica, aunque limitada en esta área, apoya la hipótesis de que el asma, por medio del tráfico selectivo de leucocitos entre los diferentes sitios y la mucosa glandular del cuerpo, puede tener los mismos efectos fisiopatológicos en el estómago y las vías respiratorias. Este estudio tuvo como objetivo determinar si el asma, en ausencia y presencia de diversos tratamientos para el asma (hidrocortisona y Modul8 TM), generó alguna alteración morfológica en las céluals parietales y principales del estómago. El modelo murino BALB/c del ratón asmático fue el modelo de elección en este estudio. El protocolo de inducción de asma, así como el tratamiento del asma demostró ser eficaz con la ayuda de lavado bronquial y cuantificación leucocitaria del fluido. Biopsias de las regiones fúndica y pilórica fueron extraídas y evaluadas por medio de microscopía electrónica de transmisión, de barrido y de luz. Las biopsias extraídas de la región fúndica y pilórica revelaron que el asma solamente induce hipertrofia de las células parietales (aumento del tamaño de las células parietales P <0,00001 en ambas regiones del estómago) e hiperfuncionamiento de las células principales. El uso de hidrocortisona y Modul8 TM, como una terapia para corregir las alteraciones gástricas fue disimil, sólo en el caso de las células parietales fúndicas ambos tratamientos fueron capaces de compensar el efecto hipertrófico causado por el asma, mientras que en la célula parietal pílorica la hipertrofia inducida por el asma solamente se vio compensada por Modul8TM.

Concerns on Atrophic Gastritis and Neoplasia: Unsafe Perspective / 대한내과학회지

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.

Effect of mica monomer powder on chief and parietal cells as well as G and D cells in gastric mucosa of chronic atrophic gastritis in rats / 中国结合医学杂志

<p><b>OBJECTIVE</b>To 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.</p><p><b>METHODS</b>Intervention 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.</p><p><b>RESULTS</b>Mica 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.</p><p><b>CONCLUSION</b>Mica 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.</p>

Investigations proposed to accurately classify chronic gastritis.

Patients of chronic gastritis should be investigated with gastric mucosal biopsy, parietal cell antibody, intrinsic factor antibody, Helicobacter pylori antibody, urea breath test or faecal antigen test for Helicobacter pylori, to accurately classify them. The results of these tests will indicate Helicobacter pylori infection (present or past), the role of hereditary factor (intrinsic factor antibody present or absent) and the success or failure of Helicobacter pylori eradication treatment.

Selective COX-2 inhibitor delays experimental gastric ulcer healing by stimulating gastric acid secretion in rats / 南方医科大学学报

<p><b>OBJECTIVE</b>To 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.</p><p><b>METHODS</b>Gastric 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.</p><p><b>RESULTS</b>Nine 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.</p><p><b>CONCLUSION</b>Selective 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.</p>

Protective effect of nitric oxide on gastric mucosa and its relationship to the acid secretion of gastric parietal cells under stress in rats / 中国应用生理学杂志

<p><b>AIM</b>To 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.</p><p><b>METHODS</b>Water 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.</p><p><b>RESULTS</b>L-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.</p><p><b>CONCLUSION</b>Endogenous nitric oxide plays an important role in protecting gastric mucosa from stress-induced lesion by inhibiting H+, K(+) -ATPase activity of parietal cells.</p>

Estudo histológico e computadorizado das áreas com células parietais e principais no estômago de ratos Wistar tratados com pantoprazol e N-Nitroso-N-Methylurea (NMU) / Histological and computer study with parietal and chief cells stomach areas in Wistar rats treated with pantoprazole and N-Nitroso-N-Methylurea (NMU)

O uso prolongado dos inibidores da bomba de prótons tem sido considerado uma condição de risco para o desenvolvimento de gastrite atrófica e tumores gástricos. Objetivo: Estudar o efeito do uso de pantoprazol (PTZ) e carcinogênese pela "N-Nitroso-N-Methylurea" (NMU), por 15 semanas, sobre o estômago glandular de ratos Wistar, pela análise histológica e computadorizada das áreas com células parietais (AP), principais (AZ) e da mucosa não oxíntica (ANO), além do estudo das alterações histopatológicas identificadas. Métodos: Quarenta ratos Wistar machos foram distribuídos em 4 grupos: G1 (controle), G2 (NMU+PTZ), G3 (PTZ) e G4 (NMU). O pantoprazol foi administrado 2x/semana (14mg/kg de peso, i.p.) e a NMU oferecida, ad libitum, diluída na água de beber (100mg/ml). Após o estudo histológico AP, AZ e ANO foram determinadas por análise computadorizada das imagens dos estômagos, utilizando o programa "ImageJ 1.19z". Resultados: Mostraram redução da AP e aumento da ANO, em G2, G3 e G4 (p<0,001). Foram encontrados casos de atrofia, inflamação aguda e inflamação crônica, em número que impediu comparação estatística entre os grupos estudados. Conclusão: O uso contínuo de pantoprazol (i.p.), por 15 semanas, reduziu a área com células parietais e aumentou a área de mucosa não oxíntica no estômago glandular de ratos Wistar machos. O mesmo aconteceu no grupo de animais que receberam NMU isoladamente ou em associação com o pantoprazol.

Ultrastructural Alterations Induced by 5-Fluorouracil or Mitomycin C on the Gastric Parietal Cells of Mouse / 대한해부학회지

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.

Effects of BCG or AG60 on Gastric Parietal Cells of the Mouse Implanted with Ehrlich Carcinoma Cells / 대한해부학회지

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.

Morphological Adaptive Responses of Gastric Parietal and Colonic Surface Epithelial Cells to Chronic Changes in Dietary Potassium / 대한해부학회지

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.

Gastric Adaptive Responses to Chronic Hypokalemia / 대한해부학회지

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.

Fisiología gástrica / Gastric physiology

La secreción gástrica, como cada una de las funciones de nuestro organismo, requiere de una compleja integración de mecanismos neurales y endocrinológicos. El nervio vago y el sistema nervioso entérico, así como tres diferentes tipos de células (G, D, ECL) participan en la regulación de la función gástrica. La histamina es el principal secretagogo y tanto la vía nerviosa como la gástrica controlan la secreción de la misma. Esta sustancia actúa en receptores H2 que están unidos a proteína Gs, la cual activa a la adenilciclasa para que produzca AMPc y excite a la proteincinasa-C, que a su vez fosforila a la H+/K+ ATPasa. En esta revisión analizamos estos mecanismos.

Isolated gastric mucosal cells: a model for gastric injury induced by bile acids

The current study examined the deleterious effect of glycocholic [GC] and deoxycholic acids [DC] exposure of isolated gastric mucosal cells in culture. Bile salts were known to be injurious to gastric mucosa. Dispersed gastric cells were obtained from rabbit gastric mucosa by collagenase digestion technique. Freshly isolated gastric cells were exposed to 0.2, 0.5 and 1.0 mmol/L of glycocholic and deoxycholic acids for period of up to 45 minutes in C-199 medium with 10% fetal bovine serum [FBS] [pH 7.0-7.4]. Control cell suspension was exposed to salt solution phosphate buffer saline [PBS++] without DC or GC. An attempt to establish long cell culture model was not successful as the isolated gastric cells rapidly lose their characteristic phenotypes and convert into fibroblast-like cells within one week in culture, in spite their continuous expression of cytokeratin of epithelial cells. Ultrastructural changes of timed series of samples were observed. Widespread epithelial and endothelial cells changes were seen. The most prominent alteration was degranulation of apical mucin secreting cells and excessive cytoplasmic vesiculation. The zymogen secreting cell appeared more resistant to bile salts effect, whereas the parietal cells showed excessive breaking of intracellular canaliculi [ICC]. The enteroendocrine cells exhibited loss of mitochondrial cristae, loss of their granulations, cytoplasmic vesiculation and lipid accumulation