Kivilaakso E, Ehnholm C, Kalima T V, Lempinen M
Surgery. 1976 Jan;79(1):65-9.
The role of duodenogastric reflux of lysolecithin, a normal constituent of duodenal juice, in the pathogenesis of gastric stress ulcerations was investigated with a swine shock-ulcer model. Twenty-seven piglets, weighing 8 to 12 kilograms, were used. In an intact animal, the average concentration of intragastric lysolecithin before shock was 138 mug per milliliter (median, N = 6). At the end of the shock period, the average concentration of lysolecithin was 540 mug per milliliter and the over-all amount in the gastric juice was 14.3 mg. (median, N = 6). Following hemorrhagic shock (3 hours duration; mean arterial pressure, 40 mm. Hg), all six control animals with normal gastroduodenal continuity got gastric ulcerations. Interruption of duodenogastric reflux by duodenal exclusion and gastrojejunostomy completely abolished the development of these ulcerations in six test animals. When the interrupted duodenogastric reflux was replaced artificially by intragastric instillation of lysolecithin (500 mug per milliliter; 25 ml.), all six animals developed lesions. Intragastric lysolecithin without shock had no effect. The results provide further support to the concept that regurgitation of duodenal juice into the stomach is an essential factor in the pathogenesis of gastric stress ulceration. The results also suggest that, in this respect, one of the active components in duodenal juice is lysolecithin.