FOCAL MICRO-CIRCULATORY CHANGES DURING THE PRODUCTION OF ASPIRIN-INDUCED GASTRIC-MUCOSAL EROSIONS

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  • 1 January 1981
    • journal article
    • research article
    • Vol. 89  (3) , 337-341
Abstract
Ischemia of the gastric epithelium has emerged as one of the more likely mechanisms for gastric ulceration. Radiolabeled microspheres (15.mu.) were used to measure blood flow to exteriorized, chambered stomach segments in 8 dogs during the development of aspirin erosions. Flow determinations were made before aspirin (20 mM in 140 mM HCl) exposure and at 2, 10 and 20 min after the initiation of the chemical insult. Lesions formed at 30 min of acetylsalicylic acid exposure. The epithelium was separated into normal and injured, based on gross discoloration caused by intramucosal hemorrhage. The calculated blood flows to the abnormal and normal mucosa were identical at 2 min (0.22 .+-. 0.04 vs. 0.15 .+-. 0.03) and at 10 min (0.39 .+-. 20 vs. 0.17 .+-. 0.04) after initiation of aspirin injury (all values in ml/g-wet wt per min, mean .+-. SEM [standard error of mean]). By 20 min of aspirin exposure, mucosal blood flow to areas that eventually became injured was greater than the blood flow to areas that remained normal (0.45 .+-. 0.12 vs. 0.13 .+-. 0.05 P < 0.05). Ischemia does not play a role in chemical erosive gastritis.