Charles Bowesman, O.B.E., B.A., M.D., F.R.C.S.E., F.A.C.S., D.T.M.&H., Editor. 1st edition, 1068 + viii pages, illustrated. Edinburgh and London, E. & S. Livingstone Ltd. (The Williams & Wilkins Co., Baltimore, exclusive U.S. agents), 1960. $22.50
This study tested the hypothesis that the inhibitory action of secretion on gastrin-stimulated gastric acid and pepsin secretion is compromised in animals harboring intestinal stages of the parasite Trichinella spiralis. Pentagastrin-stimulated acid and pepsin secretion, and the influence of secretin on these processes, were measured in dogs prepared with gastric fistulas and Heidenhain pouches. Dogs were studied before and after infection with 104T. spiralis larvae/kg body weight. Gastric secretion was stimulated by constant intravenous infusion of pentagastrin, 1 µg/kg per hour. Exogenous secretin inhibited pentagastrin-stimulated acid and pepsin output from both the main stomach and Heidenhain pouch in infected as well as in the uninfected dogs. Identical inhibition was observed in uninfected dogs during duodenal infusion with HCl to release endogenous secretin. In contrast, duodenal stimulation with HCl did not inhibit acid and pepsin secretion in dogs tested during the 1st week following infection. Results support the conclusion that the regulatory effect of secretin on gastrin-stimulated gastric secretion is impaired during the early phase of infection, and is due to depressed synthesis or release of secretion from duodenal mucosa.
Present address: Department of Physiology, Medical School in Cracow, 31-531 Cracow, Grzegorzeka 16, Poland.