The effects of a gastric inhibitory substance on gastric secretion in the pylorus ligated rat.
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In five conscious dogs motility of the antrum, pyloric sphincter, and duodenum was recorded with strain gauge transducers and induction coils. Gastric evacuation of low, medium, and high viscosity meals was measured via a duodenal cannula and observed simultaneously by radiography. Computer analysis of the propagation of the gastric waves revealed increased velocity in the distal antrum but no simultaneous contractions of the terminal antrum and pyloric sphincter. Radiography showed, and measurements of the antral diameter confirmed, that the indentations of the gastric waves were significantly deeper with the low viscosity liquid meal compared with the medium and high viscosity meals. Thereby, retropulsion of the medium and high viscosity ingesta was produced. Results indicated that gastric evacuation was regulated predominantly by the depth of the peristaltic indentation, which depended on the viscosity of the gastric contents. Nothing indicated that the phasic contractions of the pyloric sphincter were of importance for the regulation of gastric emptying.
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Rats pre-fed on a South Indian diet show a much higher incidence of ulceration of the stomach after pyloric ligation than those on a North Indian diet. Removing vegetables and pulses from the North Indian diet deprives it of its protective effect. Staple foodstuffs with a high buffer content (unmilled rice, unrefined wheat and a millet [ragi]) placed in the stomach after pyloric ligation are also protective, but those with a low buffer content (milled rice, tapioca, sorghum and maize) are not protective. Refined wheat, however, gives protection despite its low buffer content. The significance of these findings in relationship to the distribution of duodenal ulcer in India and Africa is discussed.
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Antropyloroduodenal motility was recorded in seven anesthetized dogs to assess the role of nitric oxide and L-arginine metabolites in nonadrenergic noncholinergic (NANC) mediation of pyloric relaxation. Pyloric activity induced by duodenal field stimulation was inhibited by antral field stimulation and electrical vagal stimulation. Intra-arterial NG-L-arginine-methyl-ester (L-NAME) reduced the inhibition from antral or vagal stimulation (P less than 0.05). Intravenous infusion of L-NAME also blocked the inhibitory effect of vagal and antral stimulation but left the tetrodotoxin-insensitive action of intra-arterial vasoactive intestinal peptide (VIP) and sodium nitroprusside unchanged. L-Arginine reversed the effect of L-NAME whereas D-arginine did not. L-NAME enhanced pyloric contractions to intra-arterial acetylcholine. The NANC inhibition of the substance P-stimulated pyloric response in vitro was blocked by L-NAME and reversed by addition of L-arginine. Sodium nitroprusside was effective as a relaxant in vitro but VIP was not. These data suggest that metabolites of L-arginine mediate neural inhibition of canine pyloric motor activity.
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