Effect of 50% small bowel resection on gastric prostaglandin E2 levels in rats

The mechanism for the production of increased gastric secretion following massive intestinal resection is not clearly defined. The loss of an intestinal inhibitor has been most frequently suggested to explain this hypersecretion. The role of endogenous prostaglandins which can inhibit gastric secretion is not established. The present study was undertaken to determine the effect of 50% proximal small bowel resection on Prostaglandin E2 (PGE2) levels in rat gastric mucosa. This study was performed in 30 rats divided into three groups. The first group of rats served as unoperated controls, the second group was sham operated and the third group underwent 50% resection of proximal small intestine. The PGE2 levels in rat gastric mucosa was decreased significantly (p < 0.001) in the resected group (422.85 +/- 7.66 pg/gm) as compared with the sham group (478.77 +/- 7.25 pg/gm) and the control group (493.38 +/- 4.61 pg/gm). Total gastric acidity was increased significantly (p < 0.001) in the resection group (63.05 +/- 2.64 mEq/L) as compared with the sham group (15.21 +/- 0.99 mEq/L) and the control group (17.19 +/- 0.80 mEq/L). The PGE2 levels and total gastric acidity were not significantly changed in either the control or sham operation groups (p > 0.05). The results suggest that endogenous prostaglandin synthesis has a regulatory role in gastric hyperacidity after 50% proximal small bowel resection in rats.