Prostanoid production in post-gastrectomy gastritis: Influence of sucralfate

Abstract

Prostaglandins seem to play an important role in the protection of the gastric mucosa, but the effect of cytoprotective drugs such as sucralfate on prostaglandin synthesis and in the prevention of gastritis induced by gastric surgery has not been definitely established. The purpose of this study was to determine: (1) the prostanoid production and the histologic changes occurring after various surgical techniques in rat gastric mucosa; and (2) the influence of sucralfate treatment on prostanoid levels and gastric damage induced by gastric surgery. Animals included in the study had undergone one of three surgical procedures: Billroth I, Billroth II, or truncal vagotomy plus pyleroplasty. Animals that had no surgery and “sham-operated” animals were used as controls. One third of the animals in each group received sucralfate treatment (an average of 100 mg/kg per day). Samples of gastric mucosa were taken after one year, and prostaglandin E 2 (PGE 2), 6-keto-PGF 1α, and thromboxane B 2 synthesis were measured by radioimmunoassay. The sucralfate-treated group consistently showed higher PGE 2 and 6-keto-PGF 1α values and a higher 6-keto-PGF 1α:thromboxane B 2 ratio, as well as lower thromboxane B 2 levels than untreated animals, although the differences were statistically significant only in the 6-keto-PGF 1α:thromboxane B 2 ratio. Similarly, gastritis was more frequent and more severe in the untreated animals. In conclusion, sucralfate seems to provide protection against gastritis induced by gastric surgery and increases the 6-keto-PGF 1α:thromboxane B 2 ratio.