Neonatal bacterial attack-unraveling the mysteries of acid defense

2021 ◽  
Vol 10 ◽  
pp. 27
Author(s):  
Ian Munro Rogers
Keyword(s):  
Acid Secretion ◽  
Negative Feedback ◽  
Gastric Acidity ◽  
Review Article ◽  
Maternal Transfer ◽  
Bacterial Attack

This review article examines how gastric acidity develops and is maintained during the first 4 weeks of life. An initial maternal transfer of gastrin is followed by progressively increasing baby gastrin, not yet restrained by the rising acidity. When the negative feedback matures, baby acid secretion becomes controlled and independent.

scholarly journals Starting from scratch: The primary hyperacidity theory of the cause of pyloric stenosis of infancy

2022 ◽  
Vol 11 ◽  
pp. 7
Author(s):  
Ian Munro Rogers
Keyword(s):  
Family History ◽  
Clinical Features ◽  
Pyloric Stenosis ◽  
Negative Feedback ◽  
Gastric Acidity ◽  
Modern Technology ◽  
Male Predominance

The early observations of those who first described babies with pyloric stenosis (PS) are used as a backdrop for the development of the Inherited Primary Hyperacidity theory of cause. Those early truths, uncomplicated by modern technology, have acted as a springboard for pathogenesis. Hyperacidity, male predominance, family history, self-cure, enhanced appetite, and time-sensitive presentation were all well known to the early pioneers. Any system of pathogenesis must explain all these clinical features. The Inherited Primary Hyperacidity theory does this and is a credible explanation for all the clinical features established by these early pioneers. The evidence which supports a delay in maturation of the negative feedback between gastrin and gastric acidity is presented. Such a phenomenon further supports the Primary Hyperacidity theory.

scholarly journals Antisecretory Action of the Extract of the Aerial Parts ofEremomastax speciosa (Acanthaceae)Occurs through Antihistaminic and Anticholinergic Pathways

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Amang André Perfusion ◽  
Paul V. Tan ◽  
Nkwengoua Ernestine ◽  
Nyasse Barthélemy
Keyword(s):  
Gastric Secretion ◽  
Acid Secretion ◽  
Aqueous Extract ◽  
Gastric Acidity ◽  
Gastric Volume ◽  
Gastric Ulceration ◽  
Mucus Production ◽  
Aerial Parts ◽  
Antisecretory Effect ◽  
Pylorus Ligation

Objective.The objective of this study was to find out the possible antiulcer mechanism of action ofEremomastax speciosa.Method.Carbachol- and histamine-induced hypersecretion, associated with the pylorus ligation technique, were used in rats. Gastric mucosal ulceration, mucus production, pH, gastric volume, and acidity were measured.Results.Histamine and carbachol raised gastric acidity to 86.50 and 84.80 mEq/L, respectively, in the control rats, and the extracts (200 mg/kg) reduced gastric acidity to 34.60 and 39.00 mEq/L, respectively. Intraduodenal aqueous extract (400 mg/kg) in histamine- and carbachol-treated rats produced significant (P<0.001) decreases in acid secretion to 28.50 and 28.80 mEq/L, respectively, and 100 percent inhibition of gastric ulceration. Augmented histamine-induced gastric acid secretion (90.20 mEq/L) was significantly reduced to 52.60 and 27.50 mEq/L by the 200 and 400 mg/kg doses of the aqueous extract, respectively. The extract significantly reduced (P<0.001) the volume of gastric secretion and significantly increased mucus production. The ulcer inhibition potential of the extract significantly dropped to 25–44% (oral extract) and to 29–37% (duodenal extract) in carbachol/indomethacin-treated rats.Conclusion.The aqueous extract ofE. speciosahas both cytoprotective and antisecretory effects. The antisecretory effect may involve a mechanism common to both cholinergic and histaminergic pathways.

scholarly journals Review article: methods of measuring gastric acid secretion

2011 ◽  
Vol 33 (7) ◽  
pp. 768-781 ◽  
Author(s):  
T. Ghosh ◽  
D. I. Lewis ◽  
A. T. R. Axon ◽  
S. M. Everett
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Review Article

Influence of H. pylori infection on meal-stimulated gastric acid secretion and gastroesophageal acid reflux

1999 ◽  
Vol 277 (6) ◽  
pp. G1159-G1164 ◽  
Author(s):  
Mark Feldman ◽  
Byron Cryer ◽  
Doug Sammer ◽  
Edward Lee ◽  
Stuart J. Spechler
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Persistent Infection ◽  
Gastric Acidity ◽  
Acid Reflux ◽  
Gastrin Release ◽  
Before And After ◽  
H Pylori

Gastric acid secretion, gastrin release, gastric emptying, and gastroesophageal acid reflux were measured in asymptomatic individuals before and after elimination of Helicobacter pylorigastritis. After basal gastric acid secretion and serum gastrin concentrations were measured, meal-stimulated gastric acid secretion and gastrin release were assessed during in vivo intragastric titration to pH 3. Experiments were repeated 4 wk after treatment with lansoprazole, amoxicillin, and clarithromycin. Esophageal pH was also monitored for 24 h before and after therapy. Basal gastric acidity increased ∼20 mmol/l in subjects whose infection was eradicated ( P < 0.05) but not in those with persistent infection. Basal and meal-stimulated gastric acid secretion did not change after H. pylorieradication, despite a 41% reduction in meal-stimulated gastrin release ( P < 0.05). Gastroesophageal acid reflux increased two- to threefold after successful treatment ( P < 0.05) but did not change in subjects with persistent infection. Thus elimination of H. pylori gastritis increases gastric acidity, probably by reducing nonparietal alkaline secretion, and this may facilitate gastroesophageal acid reflux.

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