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At least 397 records · Page 22Linked to original sources
PubMed1993

Mucosal secretion and cytoprotection of the rat gastric mucosa.

We carried out a series of experiments to test the hypothesis that many examples of gastric cytoprotection result from the ability of protective agents to elevate mucosal secretion. Specifically, such protection would be effective against barrier breakers that act directly on the mucosal surface. We have previously observed that the protection found to result, in our rat gastric chamber model, from luminal stasis or from sucralfate, was accompanied by increases in the thickness of a juxtamucosal pH gradient. The pH gradient was measured with antimony microelectrodes and was about 900 microns thick over chambered gastric mucosae that had not had the luminal solution stirred for at least 5 min. When the solution was stirred (200 rpm) for 10 min with a plastic paddle, the thickness of the pH gradient was decreased to about 400 microns but recovered to more than 90% of the starting value within 5 min. The thickness of the pH gradient varied from site to site, with a range from about 500 microns to 1,800 microns. However, the thickness was constant at a given site when it was remeasured after about 1 h. Capsaicin at a concentration of 640 microM rapidly increased both gastric blood flow and the thickness of the juxtamucosal pH gradient by about 50%. However, 25 min after removal of the capsaicin the gastric blood flow approached pre-capsaicin levels, and the thickness of the gradient remained increased by nearly 50%. In a third set of experiments, the vulnerability of specific sites on the chambered mucosae to acidified sodium taurocholate was correlated with the thickness of the juxtamucosal pH gradient before exposure to taurocholate.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1977

Effect of histamine H2 antagonism by metiamide on the response of the canine gastric mucosa to acid and bile salt.

Prevention of acute gastric erosions with histamine H2-receptor blocking agents suggests that these drugs may improve the ability of the gastric mucosa to maintain electrical, ionic, and protein concentration gradients. In 5 awake mongrel dogs, transmural potential difference, ion fluxes, and protein loss were measured across Heidenhain pouches topically exposed to isotonic solutions containing either 80 mM HCl or 80 mM HCl plus 20 mM sodium taurocholate (BS). The dogs received an intravenous infusion of either saline (as a control) or the H2 antagonist metiamide, 10 mumoles per kg-hr. Metiamide increased the H+ clearance rate found after acid test solution exposure but had no significant effect on potential difference or ion fluxes. H2 antagonism decreased the protein loss but not the increase in cation permeability due to BS. Net H+ loss actually increased, which, along with a decrease in Cl- gain, suggests inhibition of acid secretion by metiamide in BS-exposed gastric mucosa. These effects of metiamide point to histamine as a likely mediator of the gastric mucosal damage due to BS.

Animals↗
PubMed1981

Gastric acid response to topical or intravenous histamine and topical H2-receptor blockade in dogs.

This study was undertaken to determine gastric acid surface and to examine the local effect f ranitidine, a histamine H2-receptor antagonist, on the gastric acid response to histamine. Histamine applied to the Heidenhain pouch (HP) mucosa resulted in a slight and dose-dependent stimulation of acid secretion without affecting acid secretion from the main stomach. Ranitidine given into the HP caused dose-dependent inhibition of the HP response to topical or intravenous histamine without affecting the acid response of the main stomach and without any significant change in the serum ranitidine level. Ranitidine applied to the main stomach with the pylorus occluded inhibited histamine-induced acid secretion also without any increase in the serum ranitidine level. This inhibition was about 30% of that obtained with the same dose of ranitidine given into the stomach with the pylorus left open during the experiment. This study provides evidence that topical histamine is a weak stimulant of gastric secretion and that topical ranitidine is capable of local inhibition of the acid response to both topical and intravenous histamine.

Administration, Topical↗