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The effects of an amino acid, L-glutamine, on aspirin-induced gastric lesions and gastric secretion were studied in either intact or pylorus-ligated rats. L-Glutamine had a pronounced inhibitory effect on gastric lesions induced by aspirin administered by oral, intraperitoneal, or intraduodenal routes to intact or pylorus-ligated rats. By the oral route the inhibition was dose-related. However, L-glutamine given either intraduodenally or intraperitoneally did not show any appreciable effects on gastric lesions induced by orally administered aspirin in pylorus-ligated rats. One mechanism of L-glutamine protection was inhibition of a back diffusion of gastric acid caused by aspirin and this was demonstrated in pylorus-ligated rats. The reduction in H+and increase in Na+concentrations in the lumen caused by aspirin was returned to normal by increasing doses of L-glutamine. In addition, L-glutamine was considered to inhibit the back diffusion of acid caused by pylorus ligation per se, because the amino-acid produced an increment of H+and reduction of Na+and K+in comparison with the control group. The role of pepsin on L-glutamine protection was negligible.

Isoamyl acetate, n-butyl acetate, n-amyl acetate and n-propyl acetate produced contractions of the isolated ileum of the guinea-pig. These were inhibited by atropine, procaine and by cooling. These acetates and also s-butyl, t-butyl and n-octyl acetate behaved as inhibitors of acetylcholine at 14 ± 1°. The acetylcholine content in the organ bath fluid increased after 60 min incubation of the ileum with isoamyl acetate. The results indicated that the agonistic acetates produced contraction of ileum through the liberation of acetylcholine from the cholinergic nerve-endings. All the acetates behaved as inhibitors of acetylcholine when they combined with the acetylcholine receptor on the muscle.

The effects of papaverine, isoprenaline and N6,2′-O-dibutyryl 3′,5′-cyclic adenosine monophosphate (DiBu.C-AMP) on calcium movements in the taenia from the guinea-pig caecum have been investigated and compared with the effects of phenylephrine. Papaverine and DiBu.C-AMP antagonized the contraction of KCl-depolarized muscle induced by CaCl2and increased 45Ca-efflux from the taenia. Papaverine also significantly depressed 45Ca-uptake by this preparation. These findings suggest that papaverine impairs the availability of calcium to the contractile system and that there may be a correlation between relaxation and increase of 45Ca-efflux. The action of DiBu.C-AMP resembles that of papaverine but its potency is less.