The Effect of Intragastric Ammonia Production on Titratable Gastric Acid Output in Helicobacter pylori-Infected Patients with Chronic Gastritis

2005 ◽  
Vol 50 (11) ◽  
pp. 2094-2099 ◽  
Author(s):  
Bogdan Cylwik ◽  
Jan W. Dlugosz ◽  
Andrzej Kemona ◽  
Maciej Szmitkowski
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Acid ◽  
Chronic Gastritis ◽  
Acid Output ◽  
Ammonia Production ◽  
Gastric Acid Output

scholarly journals Helicobacter pylori infection potentiates the inhibition of gastric acid secretion by omeprazole

Gut ◽  
1999 ◽  
Vol 44 (4) ◽  
pp. 468-475 ◽  
Author(s):  
D Gillen ◽  
A A Wirz ◽  
W D Neithercut ◽  
J E S Ardill ◽  
K E L McColl
Keyword(s):  
Helicobacter Pylori ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Acid Output ◽  
Intragastric Ph ◽  
Ammonia Production ◽  
Intragastric Acid ◽  
H Pylori

BACKGROUNDOmeprazole has a greater intragastric pH elevating effect in Helicobacter pylori positive than negative subjects. Ammonia production byH pylori has been suggested as a probable mechanism.AIMSTo assess the effect ofH pylori status on gastric acid secretion during omeprazole treatment, and to examine the possible role of ammonia neutralisation of intragastric acid in increased omeprazole efficacy in infected subjects.METHODSTwentyH pylori positive and 12H pylori negative healthy volunteers were examined before and six to eight weeks after commencing omeprazole 40 mg/day. On both occasions plasma gastrin and acid output were measured basally and in response to increasing doses of gastrin 17 (G-17). Gastric juice ammonium concentrations were also measured.RESULTSPrior to omeprazole, measurements were similar in the H pyloripositive and negative subjects. During omeprazole, median basal intragastric pH was higher in the H pyloripositive (7.95) versus negative (3.75) subjects (p<0.002). During omeprazole basal, submaximal (180 pmol/kg/h G-17), and maximal acid outputs (800 pmol/kg/h G-17) were lower in H pylori positive subjects (0.0, 3.6, 6.0 mmol/h respectively) versus negative subjects (0.3, 14.2, 18.6 mmol/h) (p<0.03 for each). This effect was not explained by neutralisation by ammonia.CONCLUSIONThe presence ofH pylori infection leads to a more profound suppression of acid secretion during omeprazole treatment. The effect cannot be explained by neutralisation of intragastric acid by bacterial ammonia production and its precise mechanism has to be explained.

Gastric acid output, bacterial load and gastritis in Helicobacter pylori positive patients with duodenal ulcer

1995 ◽  
Vol 108 (4) ◽  
pp. A147
Author(s):  
PH Le Roux ◽  
AW Harris ◽  
MM Walker ◽  
JJ Misiewicz ◽  
JH Baron
Keyword(s):  
Duodenal Ulcer ◽  
Helicobacter Pylori ◽  
Gastric Acid ◽  
Acid Output ◽  
Bacterial Load ◽  
Gastric Acid Output

scholarly journals Relation between gastric acid output, Helicobacter pylori, and gastric metaplasia in the duodenal bulb.

Gut ◽  
1996 ◽  
Vol 39 (4) ◽  
pp. 513-520 ◽  
Author(s):  
A W Harris ◽  
P A Gummett ◽  
M M Walker ◽  
J J Misiewicz ◽  
J H Baron
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Acid ◽  
Acid Output ◽  
Duodenal Bulb ◽  
Gastric Acid Output ◽  
Gastric Metaplasia

scholarly journals Sexual arousal increases gastric acid output

1978 ◽  
Vol 74 (5) ◽  
pp. 1066
Author(s):  
J.C. Meeroff
Keyword(s):  
Gastric Acid ◽  
Sexual Arousal ◽  
Acid Output ◽  
Gastric Acid Output

scholarly journals PAC1 Deficiency in a Murine Model Induces Gastric Mucosa Hypertrophy and Higher Basal Gastric Acid Output

2010 ◽  
Vol 43 (1) ◽  
pp. 76-84 ◽  
Author(s):  
Yuxin Lu ◽  
Patrizia Germano ◽  
Gordon V. Ohning ◽  
John P. Vu ◽  
Joseph R. Pisegna
Keyword(s):  
Gastric Mucosa ◽  
Gastric Acid ◽  
Murine Model ◽  
Acid Output ◽  
Gastric Acid Output

Effect of vagotomy on the acid response to gastric distension

1970 ◽  
Vol 48 (10) ◽  
pp. 670-674 ◽  
Author(s):  
R. M. Preshaw
Keyword(s):  
Motor Activity ◽  
Gastric Acid ◽  
Motor Response ◽  
Acid Output ◽  
The Body ◽  
Conscious Dogs ◽  
Truncal Vagotomy ◽  
Gastric Distension ◽  
Gastric Acid Output

Distension of the body of the stomach, in conscious dogs with vagally innervated antral pouches, caused an increase in gastric acid output, and an increase in antral motor activity. Truncal vagotomy inhibited the acid response to distension, but had no effect on the antral motor response. Denervation of the antral pouch by separating it from the main stomach caused little further diminution in the response.

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