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Abstract
This study was designed to establish the role of tissue phospholipase (PLase) and prostaglandins (PGs) in the genesis of gastric ulcers. The activity of PLase and levels of PGs in rat gastric mucosa were measured by high-performance liquid chromatography, using water immersion stress ulcer. Four kinds of PGs in gastric mucosa were determined: 6-keto-PGF1α, PGF2α, PGE2, and PGD,. Decreases in PG levels and in PLase activity were observed, depending on the duration of vater immersion stress. Either administration of pirenzepine or vagotomy maintained both the PG levels and PLase activity. The longer duration of stress induced a more severe ulcer index. Premedication with pirenzepine or vagotomy prevented ulceration. Furthermore, there was a clear reciprocal correlation between the PLase activity and the ulcer index. The decrease in PG levels observed could be linked with the decrease in the activity of PLase, the initiating enzyme of the arachidonate cascade reaction. Thus, PLase might be a responsible factor in the genesis of stress ulcers. Pirenzepine or vagotomy protected gastric mucosa from ulceration by maintaining the PLase activity and PG levels.