Mechanisms of acute gastric mucosal lesion accompanying obstructive jaundice--role of bile acids in plasma.

The mechanism of acute gastric mucosal lesion (AGML) accompanying obstructive jaundice was studied in male Wistar rats, with special reference to the effect of bile acids in plasma on mucosubstances in the gastric mucosa. Following ligation of the common bile duct, total plasma level of bile acids increased 24 folds over the control level, and gastric mucosal mucus contents, measured biochemically or histochemically, significantly decreased. Effect of increased bile acids in the blood stream on the gastric mucosa was estimated by continuous intravenous administration of sodium taurocholate. After 24 hours infusion, both gastric acid output and gastric mucus contents significantly decreased. Further imposition of restraint and water immersion stress produced AGML significantly earlier than in control rats with continuous intravenous infusion of 0.9% NaCl. These data suggest that the increased plasma level of bile acids play an important role on the reduction of the gastric-mucosal defense mechanism in obstructive jaundice directly through their toxic effects, and that this easily results in the formation of AGML under additional stresses.