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1.
APMIS ; 110(11): 795-801, 2002 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-12588420

RESUMO

AIM: In the present study we evaluated the effects of gastric myenteric denervation using benzalkonium chloride (BAC) on the time for gastric emptying, as well as gastric secretion, and mucosal epithelial cell size and population in rats. METHODS AND RESULTS: Wistar rats were treated with topical serosal application of BAC to the stomach. Control animals received saline. Ninety days after surgery, gastric emptying time, gastric acid secretion and serum gastrin levels were studied. Next, the animals were sacrificed and the stomachs were removed, fixed in formalin and histologically processed for histomorphometry of the height, area and volume of the glandular portion, and volume and population of mucous, chief, parietal, G- and labelled cells. BAC animals showed a significant delay in gastric emptying and an increase in gastric acid secretion and serum gastrin levels. These animals also presented a significant reduction of myenteric neuron number, hypertrophy of parietal and chief cells, hyperplasia of G cells and an increase in the gastric mucosa area. CONCLUSION: The absence of the myenteric plexus seems to protect the stomach from the hyperplastic effects of hypergastrinemia. Gastric food stasis may act as a factor triggering morphological and functional alterations of the gastric epithelium. Although gastric food stasis is a common finding in medical practice, its physiopathological consequences are poorly understood and have not been frequently discussed in the literature.


Assuntos
Esvaziamento Gástrico , Mucosa Gástrica/fisiologia , Gastrinas/sangue , Estômago/fisiologia , Animais , Compostos de Benzalcônio , Celulas Principais Gástricas/patologia , Detergentes , Ácido Gástrico/metabolismo , Determinação da Acidez Gástrica , Mucosa Gástrica/metabolismo , Mucosa Gástrica/patologia , Células Secretoras de Gastrina/patologia , Hiperplasia , Denervação Muscular/métodos , Músculo Liso/inervação , Músculo Liso/fisiologia , Plexo Mientérico/efeitos dos fármacos , Tamanho do Órgão , Células Parietais Gástricas/patologia , Ratos , Ratos Wistar , Estômago/inervação
2.
Braz. j. med. biol. res ; 29(11): 1449-54, Nov. 1996. ilus, tab
Artigo em Inglês | LILACS | ID: lil-187204

RESUMO

Patients with the digestive form of chronic Chagas' disease exhibit abnormally increased gastrin release, possibly caused by antral gastrin cell (G cell) hyperfunction. In order to identify the mechanisms underlying this abnormality, we used an immunohistochemical method to assess the population of antral somatostatin-producing cells (D cells) in chagasic patients, since somatostatin is known to be the main inhibitory factor of gastrin secretion. Samples (N = 11) of endoscopic antral biopsies taken from 16 Chagas' disease patients and 13 control subjects were studied. Antral D and G cell populations were determined by an immunohistochemical technique using highly specific antibodies against somatostatin and gastrin. There was no significant difference between Chagas' disease and control groups regarding G cell population (number of cells/mm reported as median (range): 70.0 (23.7-247.0) vs 98.1 (52.7-169.4), P>0.10). In contrast, the number of antral D cells in Chagas' disease patients was significantly lower than in controls (l6.4 (6.9-54.4) vs 59.3 (29.6-113.8), P<0.05). Chronic superficial gastritis and infection with Helicobacter pylori were more frequent in chagasic patients than in controls, but there was no demonstrable association between these factors and the reduction of the number of antral D cells. These data suggest that reduction in the number of antral somatostatin-producing cells, which should lead to reduced inhibition of gastrin cell activity, may play a role in the increased gastrin secretion observed in Chagas' disease patients.


Assuntos
Humanos , Doença de Chagas/fisiopatologia , Gastrinas/metabolismo , Antro Pilórico/fisiopatologia , Somatostatina/imunologia , Helicobacter pylori/química
3.
Braz. j. med. biol. res ; 22(7): 889-93, 1989. tab
Artigo em Inglês | LILACS | ID: lil-83241

RESUMO

The present study examines the effect of chlorpromazine and biliary drainage in cholestatic rats. The time course of portal blood flow was studied 24,48, and 72 h and seven days after bile duct ligation. Portal blood flow decreased after 72 h. Chlorpromazine reduced biliary hydrostatic pressure in sham-operated control rats, but 24-h obstruction was sufficient to prevent this effect in cholestatic rats. The drug ameliorated the mitochondrial and cell membrane function of cholestatic rats before and after drainage. The data present further support for the role of ischemia in cholestasis


Assuntos
Ratos , Animais , Masculino , Ductos Biliares/cirurgia , Clorpromazina/farmacologia , Colestase Extra-Hepática/fisiopatologia , Circulação Hepática , Mitocôndrias Hepáticas/fisiologia , Alanina Transaminase/sangue , Drenagem , Pressão Hidrostática , Isquemia/etiologia , Ratos Endogâmicos
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