Non-specific Gastritis Correlation of Histology of Gastric Mucosa with Gastric Secretory Activity Measured by Tubeless Gastric Analysis Techniques

Author(s):  
H. L. Segal ◽  
M. L. Kelley ◽  
R. N. Charles ◽  
R. Terry
2008 ◽  
Vol 21 (1) ◽  
pp. 179-182
Author(s):  
Galina Luk'yantseva ◽  
Victor Shevchuk ◽  
Galina Kopylova ◽  
Galina Samonina ◽  
Seraphima Herman ◽  
...  

1986 ◽  
Vol 251 (4) ◽  
pp. G518-G528 ◽  
Author(s):  
M. J. Rutten ◽  
S. Ito

Relationships between morphological and electrophysiological changes with low concentrations of ethanol on in vitro guinea pig gastric mucosa were investigated. Tissues mounted in Ussing chambers allowed recording of transepithelial potential difference (PD), resistance (R), short-circuit current (Isc), and acid secretion (H+). At selected times the mucosae were processed for morphological analysis. With luminal 10% ethanol there was a decrease in PD, R, Isc, and H+ within 1 min, and they eventually went to low steady-state values between 10 and 40 min. At 1 min many surface epithelial cells lifted off from the basal lamina but were still anchored by thin basal cell processes. After 10 min in ethanol many surface cells had completely detached from the basal lamina but remained connected to adjacent cells by their junctions. Numerous cytoplasmic blebs formed on both apical and basal cell surfaces. Concurrently, there was a significant increase in microvillus length. After 40 min most of the surface cells were detached from the basal lamina as sheets forming epithelial blisters. Upon ethanol washout there was epithelial cell reattachment to the basal lamina and a return of the PD, R, and Isc to control values within 40 min. Incubation of the luminal surface with 10% ethanol for 5 h resulted in a gradual rise of the PD, R, Isc, and H+ to control values by 4 h with a coincident return of the normal mucosal morphology. These studies indicate that ethanol has reversible and possibly adaptable effects on the in vitro guinea pig gastric mucosa and that the morphological changes are closely correlated with the decline and recovery of the electrical and secretory activity of the tissue.


2020 ◽  
Vol 40 (2) ◽  
Author(s):  
Wei Liu ◽  
Liang-jun Yang ◽  
Yuan-liang Liu ◽  
Dong-sheng Yuan ◽  
Zi-ming Zhao ◽  
...  

Abstract Parietal cells of the gastric mucosa contain a complex and extensive secretory membrane system that harbors gastric H+, K+-adenosine triphosphatase (ATPase), the enzyme primarily responsible for gastric lumen acidification. Here, we describe the characterization of mice deficient in the H+, K+-ATPase α subunit (Atp4a−/−) to determine the role of this protein in the biosynthesis of this membrane system and the biology of the gastric mucosa. Atp4a−/− mice were produced by gene targeting. Wild-type (WT) and Atp4a−/− mice, paired for age, were examined at 10, 12, 14 and 16 weeks for histopathology, and the expression of mucin 2 (MUC2), α-methylacyl-CoA racemase (AMACR), Ki-67 and p53 proteins was analyzed by immunohistochemistry. For further information, phosphoinositide 3-kinase (PI3K), phosphorylated-protein kinase B (p-AKT), mechanistic target of rapamycin (mTOR), hypoxia-inducible factor 1α (HIF-1α), lactate dehydrogenase A (LDHA) and sirtuin 6 (SIRT6) were detected by Western blotting. Compared with the WT mice, hypochlorhydric Atp4a−/− mice developed parietal cell atrophy and significant antral inflammation (lymphocyte infiltration) and intestinal metaplasia (IM) with elevated MUC2 expression. Areas of dysplasia in the Atp4a−/− mouse stomach showed increased AMACR and Ki-67 expression. Consistent with elevated antral proliferation, tissue isolated from Atp4a−/− mice showed elevated p53 expression. Next, we examined the mechanism by which the deficiency of the H+, K+-ATPase α subunit has an effect on the gastric mucosa. We found that the expression of phosphorylated-PI3K, p-AKT, phosphorylated-mTOR, HIF-1α, LDHA and SIRT6 was significantly higher in tissue from the Atp4a−/− mice compared with the WT mice (P<0.05). The H+, K+-ATPase α subunit is required for acid-secretory activity of parietal cells in vivo, the normal development and cellular homeostasis of the gastric mucosa, and attainment of the normal structure of the secretory membranes. Chronic achlorhydria and hypergastrinemia in aged Atp4a−/− mice produced progressive hyperplasia and mucolytic and IM, and activated the Warburg effect via PI3K/AKT/mTOR signaling.


1983 ◽  
Vol 245 (6) ◽  
pp. G797-G807 ◽  
Author(s):  
W. Zeiske ◽  
T. E. Machen ◽  
W. Van Driessche

Transport and conductance pathways for Cl- and K+ were studied in frog gastric mucosa using noise analysis techniques. The current-noise power spectra exhibited both Cl- - and K+-dependent characteristics. In Cl- -containing solutions, reductions in Cl- transport were associated with reductions of the overall noise power. Such changes appeared to reflect the movement of Cl- through the apical (mucosal) membranes of oxyntic cells. In Cl- -free solutions a K+-dependent Lorentzian component was detected in the power spectrum when applying a mucosally or serosally directed transepithelial K+ concentration gradient. This component was enhanced by 1) stimulating the oxyntic cells with histamine and 2) appropriate voltage clamping. It was reduced by mucosal Ba2+ in resting tissues and enhanced by mucosal Ba2+ in stimulated tissues. The K+ noise measured in gastric mucosae in Cl- -free solutions appeared also to be generated at the apical membranes of oxyntic cells. This is in analogy to previous findings in other gastrointestinal epithelia with fluctuating apical K+ channels. In the gastric mucosa these channels may play a key role in the mechanism of electrogenic H+ secretion.


Parasitology ◽  
1973 ◽  
Vol 66 (2) ◽  
pp. 241-257 ◽  
Author(s):  
L. M. McLeay ◽  
N. Anderson ◽  
J. B. Bingley ◽  
D. A. Titchen

Sheep in which abomasal fundic pouches had been made were infected with Ostertagia circumcincta (150000 larvae in one sheep, 100000 in three sheep). Subsequently studies were made on pouch secretion, food intake, plasma pepsinogens and abomasal pouch secretory responses when the sheep first ate. A functional abomasal lesion was apparent within 4 days of infection judged by the changes in plasma pepsinogen levels and the sodium concentrations of abomasal contents. Whereas the secretory activity of the abomasal fundic pouches (never exposed to parasites) was maintained or increased, the pH and sodium concentration of contents taken from the infected part of the abomasum were indicative of either a failure to secrete or of a permeability reabsorptive lesion. Ultrastructural studies demonstrated that parietal cells of the pouches had the appearance of cells subjected to strong secretory stimuli, but those of infected abomasa were similar to cells of gastric mucosa subjected to agents suppressing secretion. Factors which might operate, on the one hand, to stimulate secretion from separated fundic abomasal pouches, and on the other to inhibit or modify the secretory activity of the fundic mucosa of the infected abomasa, are discussed.


1981 ◽  
Vol 240 (3) ◽  
pp. G245-G249 ◽  
Author(s):  
W. D. Rees ◽  
A. Garner ◽  
K. H. Vivian ◽  
L. A. Turnberg

Effects of sodium taurocholate on the electrical and secretory activity of amphibian gastric mucosa have been studied in vitro. Exposure of the luminal surface of fundic mucosa to high concentrations (5 X 10(-2) M) at low pH (2.0 and 3.0) produced a marked fall in potential difference and electrical resistance. At lower concentrations (10(-3) to 10(-4) M) and higher pH (7.4), taurocholate did not alter the electrical properties but significantly increased net acidification from 1.39 +/- 0.27 to 2.01 +/- 0.18 mueq . cm-2 . h-1 (means +/- SE; P less than 0.01). Pretreatment of fundic mucosa with cimetidine resulted in net alkaline secretion (0.27 +/- 0.07 mueq . cm-2 . h-1), and addition of taurocholate (10(-4) M) to the luminal surface at pH 7.4 converted net alkalinization to net acidification (0.94 +/- 0.28 mueq . cm-2 . h-1). This response was not inhibited by atropine (10(-5) M) or somatostatin (10(-6) M) but exhibited marked tachyphylaxis. Taurocholate (10(-4) M) inhibited alkaline secretion in thiocyanate-treated fundic mucosa (0.63 +/- 0.04 to 0.14 +/- 0.09 mueq . cm-2 . h-1; P less than 0.001) and in spontaneously alkaline-secreting antral mucosa (0.36 +/- 0.12 to 0.09 +/- 0.06 mueq . cm-2 . h-1; P less than 0.05), but acidification did not occur. Apparent stimulation of acid secretion and simultaneous inhibition of alkaline secretion of sodium taurocholate may play a role in the pathogenesis of mucosal damage by bile.


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