HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Harper, A. A. Articles by Smy, J. R. Search for Related Content PubMed PubMed Citation Articles by Harper, A. A. Articles by Smy, J. R.

1. The effects of intragastric hyperosmolal solutions on resting and secreting stomachs of anaesthetized cats have been studied.

2. Hyperosmolal solutions reduced acid secretion in response to histamine and gastrin. There was a significant correlation between increase in osmolality and decrease in acid response to small doses of gastrin. A continuous acid secretion produced by large doses of gastrin was not significantly reduced.

3. The loss of H⁺ from resting stomachs is related to the pH and osmolality of the instilled fluid. The loss was greatest at low pH and high osmolality, but was insufficient to account for the H⁺ loss from secreting stomachs at similar pH and osmolality.

4. The Na⁺ output into resting stomachs was increased by hyperosmolal solutions, the increase being related only to the osmolality of the solutions. For the same degree of hyperosmolality there was no difference between the sodium output into resting and secreting stomachs.

5. The H⁺ deficit associated with intragastric hyperosmolal conditions does not seem to depend upon a neural mechanism, a blood-borne hormone, or a reduction in gastric blood flow. Evidence is presented that diffusion, exchange or neutralizing mechanisms are unlikely to be responsible for the H⁺ deficit. It is suggested that inhibition of oxyntic cell activity by release of a chemical agent from the surface cells of the mucosa is the most likely explanation of the results observed.

6. The possible physiological significance of intragastric hyperosmolal inhibition of acid secretion is discussed.