Characteristics of gastric inhibition by acidification of oxyntic gland area.

Abstract

SUMMARY1. Gastric acid responses to the test meals were measured in the Heidenhain pouch, gastric and pancreatic fistula dogs, using the intragastric titration method, and monitoring the rate at which a solution of 1 0 N-NaOH had to be added to maintain the pH of the gastric content constant at preselected values ranging from 5 0 to 1.0. In this way the pH profile of the gastric acid and pepsin responses to a liver extract meal kept in the Heidenhain pouch or gastric fistula as well as to exogenous stimuli such as histamine, pentagastrin or Urecholine, could be determined.2. A liver extract meal adjusted to pH 5 0 produced a potent and pressure-related stimulation of acid secretion from the Heidenhain pouch without any change in secretion from the main stomach and pancreas or in the serum concentration of immuno-assayable gastrin.3. Graded decrease of the liver extract meal pH to below 5.0 resulted in the pH-dependent inhibition of gastric acid output, which at pH 1.0 was only about 30 % of the value attained at pH 5 0. Acid secretion from the Heidenhain pouch induced by exogenous stimuli such as histamine, pentagastrin or Urecholine also showed gradual decrease when the pH of the pouch content was decreased in sequential order from 5 0 to 1X0. This pH-dependent inhibition was accompanied by an increase in pepsin secretion.4. The pH-dependent inhibition of the Heidenhain pouch response to the liver extract meal was not altered by topical application of a local anaesthetic and atropine or by the intravenous infusion of large doses of atropine, secretin or metiamide, which were shown to cause a marked inhibition of the main stomach response to the liver meal.5. The results indicate that there is a local and gastrin-independent inhibition mechanism of gastric acid secretion activated by an acidified meal making contact with the oxyntic gland area. STANISLA W J. KONTUREK AND OTHERS

Effect of luminal pH on acid secretion from Heidenhain pouches evoked by topical and parenteral stimulants

“…In conclusion, we have confirmed our earlier finding that stimulation of acid secretion by topical stimulants decreases markedly as luminal pH decreases but we could not confirm the claim of Konturek et al (1975) that regulation of acid secretion by luminal pH was a general autoregulatory phenomenon applicable to stimulants such as histamine and gastrin.…”

“…Konturek et al (1975) confirmed our (Debas & Grossman, 1975) finding that stimulation of acid secretion by instilling liver extract into a vagally denervated pouch was highly pH-dependent, acid secretion decreasing as luminal pH decreased. Konturek et al (1975) made the additional claim that luminal pH had a similar influence on acid secretion stimulated by parenteral agents such as histamine, pentagastrin, and bethanechol. The present study, using a validated method of intragastric titration, confirms our earlier finding that stimulation by topical agents is pHsensitive but fails to confirm the claim of Konturek et al (1975) that the effect of luminal pH on acid secretion is a general autoregulatory one affecting systemic stimulants as well as topical ones.…”

“…Konturek et al (1975) made the additional claim that luminal pH had a similar influence on acid secretion stimulated by parenteral agents such as histamine, pentagastrin, and bethanechol. The present study, using a validated method of intragastric titration, confirms our earlier finding that stimulation by topical agents is pHsensitive but fails to confirm the claim of Konturek et al (1975) that the effect of luminal pH on acid secretion is a general autoregulatory one affecting systemic stimulants as well as topical ones. The findings of Konturek et al can be explained in part by the artifact that titration to an endpoint of pH 1.0 produces as demonstrated in the present study.…”

Η Επιδραση Της Κολεκτομης Σε Συνδυασμο Με Χειρουργικη Βαγοτομη Στην Εκκριση Τησγαστρινης Στους Επιμυες. (Πειραματικη Εργασια)

“…Σαν μηχανισμός αναφέρεται η απ' ευθείας δράση του οξέος στα G-κύτταρα, γιατί η δράση του εξακολουθεί και μετά τοπι κή διήθηση των νεύρων του βλεννογόνου του άντρου με τοπικό αναισθητικό 22 . Εχει δειχθεί ότι το υδροχλωρικό οξύ μπορεί και αδρανοποιεί όλους τους διεγέρτες της γαστρικής έκκρισης 87 . Ενώ η πτώση του pH στο άντρο αναστέλλει τη γαστρική έκκριση, η πρόσκαιρη αλκαλοποίηση του άντρου δε διεγείρει τη γαστρική έκκριση εάν δε συνυπάρχει κάποιος από τους γνω στούς διεγέρτες γαστρίνης 30 .…”

Η Επιδραση Της Διατασης Του Παχεος Εντερου Στη Γαστρικη Εκκριση Και Τη Γαστρινητου Ορου. (Πειραματικη Εργασια)

“…Η αλκαλοποίη ση μόνη της, όταν απουσιάζει ένας κύριος διεγέρτης της γαστρίνης, δεν προκαλεί απελευθέρωση γαστρίνης' 24 '. Έχει δειχθεί ότι οξινοποίηση του οξυντικού βλεννογόνου ανα στέλλει την έκκριση οξέος σε απάντηση σε όλα τα ερεθίσματα, συμπεριλαμβανομένων της γαστρίνης και ισταμίνης' 75 '. II) Η κένωση του στομάχου η οποία αναστέλλει τη διέγερση της γαστρικής έκκρισης' 87 '.…”