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Hyperplasia of the Gastric Mucosa Produced by Duodenal Obstruction

  • Author Footnotes
    1 Dr. Crean's present address is: Gastro-Intestinal Centre, Southern General Hospital, Glasgow, S.W.1, Scotland.
    G.P. Crean
    Correspondence
    Address requests for reprints to: Dr. G. P. Crean, Medical Research Council, Clinical Endocrinology Research Unit, 2 Forrest Road, Edinburgh 1, Scotland.
    Footnotes
    1 Dr. Crean's present address is: Gastro-Intestinal Centre, Southern General Hospital, Glasgow, S.W.1, Scotland.
    Affiliations
    Medical Research Council Clinical Endocrinology Research Unit, University of Edinburgh, Gastro-Intestinal Unit, Western General Hospital, and Department of Clinical Surgery, University of Edinburgh, Scotland
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  • Author Footnotes
    2 Dr. Hogg's present address is: Department of Surgery, Royal Brisbane Hospital, Herston, Australia.
    D.F. Hogg
    Footnotes
    2 Dr. Hogg's present address is: Department of Surgery, Royal Brisbane Hospital, Herston, Australia.
    Affiliations
    Medical Research Council Clinical Endocrinology Research Unit, University of Edinburgh, Gastro-Intestinal Unit, Western General Hospital, and Department of Clinical Surgery, University of Edinburgh, Scotland
    Search for articles by this author
  • R.D.E. Rumsey
    Affiliations
    Medical Research Council Clinical Endocrinology Research Unit, University of Edinburgh, Gastro-Intestinal Unit, Western General Hospital, and Department of Clinical Surgery, University of Edinburgh, Scotland
    Search for articles by this author
  • Author Footnotes
    1 Dr. Crean's present address is: Gastro-Intestinal Centre, Southern General Hospital, Glasgow, S.W.1, Scotland.
    2 Dr. Hogg's present address is: Department of Surgery, Royal Brisbane Hospital, Herston, Australia.
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      A marked hyperplasia of the gastric mucosa was observed in rats after partial obstruction to the gastric outflow had been produced by tying a ligature around the duodenum. The effect was characterized by increases in the weight, surface area, and mucosal volume of the fundus and antrum, and there were proportional increases in the total parietal and total peptic cell populations. These effects were interpreted to mean that obstruction had caused an increase in the number of glands in the two parts of the stomach. The results suggest that the hyperplasia was due in some way to physical distension of the stomach since all of the other changes observed could be accounted for by the increase that occurred in surface area.
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