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W D Rees

Publications and source records attributed to W D Rees.

At least 127 records · Page 7Linked to original sources
PubMed1978

Effect of mast cell degranulation on gastric mucosal damage produced by sodium taurocholate in the rat.

The source of the histamine released during damage to the gastric mucosa has been investigated in rats using perfused total gastric pouches. Two groups of rats were treated with either intraperitoneal normal saline or compound 48/80, and agent that produces mast cell degranulation, over a 5-day period. On the 5th day, total gastric pouches were prepared and connected to a perfusion circuit that enabled a 20-ml volume to be circulated through the pouches. The experiments consisted of three 30-min periods during which transmucosal potential difference was monitored and ionic (hydrogen and sodium) flux measured; standard acid solution was used in the first two periods and a taurocholate solution in the third. Sodium taurocholate produced a significant increase in ionic flux and fall in the potential difference, the magnitude of the changes being similar in the 48/80- and saline-treated groups. Histamine was released from the mucosa in significantly greater amounts during the taurocholate period, and the increase was similar in both groups of rats. Histological examination of the stomachs confirmed mast cell degranulation in the 48/80-treated groups. We conclude that the histamine released during mucosal damage is probably derived from the "nonmast cell pool" and that this histamine may play a role in mediating the mucosal damage.

Animals↗
PubMed1977

The role of histamine receptors in the pathophysiology of gastric mucosal damage.

In four canine Heidenhain pouches the net fluxes of H+ and Na+ have been examined before, during, and after instillation of sodium taurocholate into the pouch. These experiments were conducted in animals given H1 (mepyramine maleate) and H2 (metiamide) histamine antagonists, alone and in combination. Control experiments without antagonists were also conducted. In control experiments, as well as in those using the histamine antagonists separately, the usual sequence of events followed exposure to taurocholate-that is, a gain in the volume of the solution in the pouch and an increase in the fluxes of Na+ and H+ across the mucosa. In experiments in which H1 and H2 histamine antagonists were used in combination, taurocholate had very little effect on the ionic fluxes of H+ and Na+, suggesting that changes in the ionic permeability of the gastric mucosal barrier are mediated by histamine through both H1 and H2 receptor sites.

Animals↗
PubMed1976

Some minimal effects of bile acid on canine gastric mucosa in Heidenhain pouches.

The gastric mucosa in four canine Heidenhain pouches was damaged with sodium taurocholate in a concentration which was just sufficient in each dog to produce consistent changes. Solutions were placed in the pouches and changes in the volume, concentrations, and fluxes of both hydrogen ion and sodium ion were measured before and during exposure to taurocholate. Changes which occurred with taurocholate were compared with control periods; taurocholate caused a relative increase in volume of 1 ml and approximately a fourfold increase in the hydrogen ion and sodium ion concentrations and the sodium ion flux. Changes in the hydrogen ion flux were smaller and, in some experiments, insignificant. Change in the hydrogen ion flux is less sensitive than the other parameters as an indicator of minimal mucosal damage.

Animals↗
PubMed1975

The effect of an aldosterone antagonist on the protective action of carbenoxolone on the gastric mucosal barrier.

The effect of an aldosterone antagonist on the protective action of carbenoxolone sodium on the gastric mucosal barrier has been studied in three dogs with Heidenhain pouches. The net fluxes of hydrogen ion and sodium ion were measured before, during, and after contact with a 10 mM bile acid solution at pH 2, in pouches which had not been treated with drugs, in pouches treated with carbenoxolone sodium and in pouches treated with both carbenoxolone sodium and the aldosterone antagonist, spironolactone. Hydrogen ion back diffusion from, and sodium ion gain by the untreated pouch was increased by 10 mM bile acid solution. Addition to the pouches of either carbenoxolone sodium alone or carbenoxolone sodium and spironolactone reduced the hydrogen ion back diffusion after exposure to the bile acid solution. The spironolactone did not change the protective effect of carbenoxolone on the gastric mucosal barrier. Carbenoxolone did not change the increased sodium ion diffusion caused by bile.

Animals↗
PubMed1968

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