Neurogastroenterology & MotilityVolume 1, Issue 1 p. 2-4 Free Access Motility Origins Charles F. Code, Charles F. Code Del Mar, CaliforniaSearch for more papers by this author Charles F. Code, Charles F. Code Del Mar, CaliforniaSearch for more papers by this author First published: September 1989 https://doi.org/10.1111/j.1365-2982.1989.tb00137.xCitations: 2AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat References 1 Alvarez WC. The mechanics of the digestive tract. 1st ed. New York : PB Hoeber Inc., 1922. The 3rd edition of this volume was entitled, An introduction to gastroenterology, 1940. 2 Alvarez WC. Incurable physician: an autobiography. Prentice-Hall, 1963. 3 Aub JC, Wobach SB, Bailey OT. Mycosis fungoides followed fourteen years; the case of W.B. Cannon. AMA Arch Pathol 1955; 60: 535– 47. 4 Cannon WB. The mechanical factors of digestion. London: Edward Arnold. New York : Longman's Green and Co., 1911. 5 Davenport HW. Gastrointestinal physiology 1895–1975: motility. Revised edition of Handbook of Physiology. The gastrointestinal system, vol 1. Baltimore : Williams and Wilkins, 1989 (in press). Citing Literature Volume1, Issue1September 1989Pages 2-4 ReferencesRelatedInformation

Increasing quantities of HCO3 − appeared in the stomach and in gastric pouches of conscious dogs with gastric infusion of increasing concentrations of ethanol. HCO3 − appearance was closely correlated with gains of K+ and of glucose to the contents and with reductions in transmucosal potential differences, each of which is associated with increased mucosal permeability. We concluded that increased diffusion of HCO3 − through a more permeable mucosa accounted for the appearance of HCO3 − with the lower concentrations of ethanol we used (5–20%) and that bulk movement of the interstitial fluid into the contents added to HCO3 − entry with the most damaging, desquamating, concentration (40%). With the gastric contents at 100 mM HCl, an unstirred layer of mucus gel over the mucosa would need to be of greater depth than previous estimates to produce mucosal surface neutrality at the rates of HCO3 − appearance we observed. However, faster rates of HCO3 − production combined with an unstirred layer could provide significant protection to the gastric mucosa.

Physiological considerations bearing on the controlle entry into the systemic circulation of orally administered drugs in healthy man are reviewed. The most desirable site for drug absorption is the sterile portion of the small intestine, so that the time “window” available for absorption is not greater than the minimum small intestinal residence time in this segment. This appears to vary widely between individuals. Methodology for sampling intestinal content and for defining the fraction absorbed and the physical state of an administered drug are summarized. Small intestinal transit and gastric emptying rates are now estimated in man by imaging techniques using Tc99m labeled sulfur colloids. Small intestinal transit may also be estimated non-invasively by measuring breath H2 after administration of a meal containing a non-absorbable disaccharide such as lactulose, but the validity of such a method is uncertain because of the acceleration of intestinal transit by lactulose. The major determinants of small intestinal transit in the fasting state is the interdigestive motor complex. During digestion, complex neurohumoral factors influence transit. Literature values for small intestinal transit are tabulated. The biochemical and physical features of the micro-environment of the stomach and small intestine during the fasting state and digestive state are reviewed. First-pass considerations are outlined, and the need for developing physiological pharmacokinetic models stressed. Available data suggest that 2–3 hours is the maximum time available for the absorption of any drug in the sterile region of the small intestine. Therefore, future therapeutic efforts aimed at slowing absorption should probably be aimed at slowing gastric emptying, unless passage of drug into the colon is judged acceptable. For rational design of controlled entry drugs, greater cooperation between the gastroenterologist and the pharmaceutical scientist appears needed.

The investigation had two major goals: to define the progression of physiological changes associated with disruption of the gastric mucosal barrier to sodium and hydrogen and to identify the morphological correlates of the physiological alterations. Fluxes of ions and water were determined before and after treatment of oxyntic mucosa with graded concentrations of butyric acid using dogs with gastric pouches. Three phases of barrier disruption were characterized: I, acceleration of normal Na+/H+ exchange; II, neutralization of H+; III, exudation of interstitial fluid. Parallel studies assessed morphological damage associated with these phases. In Phase I, cellular bulging into the lumen and dilation of intercellular spaces were evident. Some cellular erosion and extreme intercellular dilation were prominent in Phase II. Phase III was represented by necrotic changes and desquamation. It is concluded that disruption of transport mechanisms occurs sequentially and is closely correlated with morphological signs of progressive damage.

The study was designed to determine whether the special Na+–H+ barrier function or the gastric mucosa is present in the mucosa of the small bowel and whether a gastric mucosal barrier breaker (hexanoic acid) would accelerate the fluxes of sodium in duodenum–jejunum and ileum as in the stomach. The observations were made in healthy conscious dogs with Thiry-Vella fistulae of the small bowel or Heidenhain pouches of the gastric corpus. These barrier characteristics of the stomach were completely absent in the small intestine where bidirectional Na fluxes were 5–10 times greater than in the stomach and were not accelerated by hexanoic acid as they were in the stomach.A comparison was made between the rates of absorption of hexanoic acid, sodium hexanoate, and HCl from the pouches and fistulae. The lipid-soluble fatty acid was transported at all sites more rapidly than its water-soluble sodium salt. In the stomach and ileum the H+ of HCl and sodium hexanoate were absorbed at similar slow rates. The duodenal–jejunal mucosa, however, transported H+ at rates nearly identical to those of hexanoic acid. In our tests HCl was not neutralized in duodenal contents while large quantities were neutralized in the contents of ileum.

"Histamine, that decarboxylated son of histidine" — these poetic words of Carl Dragstedt, the pharmacologist and brother of Lester, the great surgeon, express beautifully the frustrations and disappointments of all who are confirmed histamine addicts. And there are quite a few in the world today. Histamine has been one of my interests for over 40 years, and she has been a fickle mistress. She was discovered as a chemical curiosity in 1907, when she was synthesized in Germany by Windaus and Vogt.1 She was isolated from biologic sources, first from ergot and then from intestinal mucosa by Barger and Dale . . .

A graduate degree program in nutrition with clinical emphasis was established in 1951 by the Mayo Graduate School of Medicine and the Graduate School of the University of Minnesota. Originally intended for dietitians at master's degree level, the program has expanded to include students of varying backgrounds and now offers the Ph.D. degree. Students in the program spend part of their time on the Twin Cities Campus of the University of Minnesota and part of their time at the Mayo Clinic in Rochester. On the Twin Cities Campus, students complete basic courses in biochemistry, physiology, and nutrition. They participate in teaching activities of the Department of Food Science and Nutrition. At the Mayo Clinic, the clinical phases of the program are completed and research conducted under the direction of a physician investigator. The program prepares clinical nutritionists to participate in nutritional care of patients and in nutrition education of health professionals.

In healthy, consious, intact fasted dogs, infusion of pentagastrin interrupted the interdigestive myoelectric complex in the stomach and small bowel and replaced it with activity that closely resembled that seen after feeding. After bilateral transthoracic vagotomy, pentagastrin infusion still interrupted the complex but now, in addition, upon stopping the pentagastrin, a premature activity front (phase III) of the complex was also followed by a reduction in the temporal regularity of the cycles of the complex. Fewer cycles per 10 hr occurred in most dogs after vagotomy, and the complexes were not as regularly interrupted by feeding a small meal of 50 g of meat as they had been before vagotomy. The results indicate that both neural and humoral influences have a role in controlling the interdigestive motor complex of dogs.

IN 1972 Black and his associates1 introduced burimamide, the first histamine H2*-receptor antagonist. Ever since, gastroenterologists have been excited by the prospect that this substance might provide the universal inhibitor of gastric secretion that they have sought, for so long, to control gastric secretion in patients with peptic-ulcer disease. The recent development of metiamide, a more potent member of the same family of drugs, by the same workers,2 has further heightened expectations — and justifiably so. Preliminary studies are encouraging.3 But we should step back to put these developments into perspective, at least as I see them from . . .