Ischemia-reperfusion of the small intestine associated with hemorrhage and other shock states is characterized by increased microvascular permeability and mucosal barrier dysfunction. Glycoproteins play an important role as a barrier to diffusion, and some of the functions of prostaglandin E
1 (PGE
1) are related to mucosal protein synthesis. The present experiment was conducted to clarify the effect of PGE
1 on mucosal levels of glycoproteins and ATP following acute ischemia-reperfusion of the small intestine. The canine jejunum was isolated, and the blood flow was blocked for 30min with or without intravenous infusion of PGE
1. Mucosal levels of ATP, Na
+-K
+ ATPase activity, glucosamine, galactosamine, and cAMP decreased, and plasma endotoxin levels in portal blood increased, after reperfusion in the PGE
1-non-treated group. These changes were suppressed and mucosal levels of cAMP were increased by the administration of PGE
1. These results suggest that mucosal permeability increased and mucin synthesis decreased markedly following acute ischemia-reperfusion and that the administration of PGE
1 suppressed these changes by stimulation of ATP and cAMP synthesis. We also conclude that the administration of PGE
1 is useful to protect against acute ischemia-reperfusion injury in the small intestine.
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