Role of intragastric pressure, pH, and pepsin in gastric ulceration in the rat.
A method of continuous gastric perfusion with "artificial gastric juice" was used in a study of individual factors (intragastric pressure, pH, and pepsin) known to participate in the pathogenesis of peptic ulcers. This method allowed change of only one factor at a time, while the other two remained constant. The gastric mucosa of normal rats, fasted for 48 hr, was found to be resistant to the ulcerogenic effects of artificial gastric juice perfused through the stomach for 6 hr without increasing the intragastric pressure. Perfusion of hydrochloric acid (pH 1.3) under increasing pressure produced ulceration of the corpus as well as forestomach portion of the stomach. The degree of gastric ulceration paralleled increases in intragastric pressure, acidity, and pepsin proteolytic activity. Inhibition of pepsin activity by a pepsin inhibitor protected the gastric mucosa even at the very low pH of 1.3. These results demonstrate that under the experimental conditions used, hydrochloric acid alone in the absence of pepsin does not produce ulceration of the rat stomach.
D000818:Animals; D005260:Female; D005750:Gastric Juice; D006863:Hydrogen-Ion Concentration; D008031:Lignin / Q000031:analogs & derivatives / Q000494:pharmacology; D010434:Pepsin A / Q000009:adverse effects / Q000037:antagonists & inhibitors / Q000502:physiology*; D011312:Pressure; D051381:Rats; D013270:Stomach / Q000503:physiopathology*; D013276:Stomach Ulcer / Q000209:etiology / Q000503:physiopathology*
D008031:Lignin; D010434:Pepsin A