The view that ulcers of the gastro-intestinal tract are due to a local loss of resistance on the part of the mucosa to the digestive activity of the gastric juice has been prominent since the time of John Hunter, more than 150 years ago. Indeed, the term "peptic" ulcer itself is an expression of that view. Theories to explain the local loss of resistance have been many. In general, as has been pointed out,1 these have been concerned with a lowering of the normal resistance alleged to be conferred on the mucosa by such factors as a general "vital" principle, the protective action of gastric mucus, the neutralizing effect of alkaline blood in the capillaries of the mucosa, or the presence of an antipepsin in the mucosa. Recent studies, however, have tended to emphasize the immediate importance of a positive factor; namely, an increase in the amount of or
GASTRIC ACIDITY AND EXPERIMENTAL ULCER. JAMA. 1936;107(25):2052–2053. doi:10.1001/jama.1936.02770510042011
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