Contribution of prostanoids to gastric circulatory and metabolic actions of solcoseryl.

Solcoseryl, a deproteinized extract of calf blood has been used in the treatment of peptic ulcer, but the mechanisms responsible for its therapeutic properties remain elusive. The present study was designed to determine the effects of solcoseryl on gastric total (GBF) and mucosal (MBF) blood flow, gastric oxygen consumption (GVO2) and mucosal formation of prostaglandin E2 (PGE2) and leukotriene C4 (LTC4) in anesthetized dogs. Soloseryl given iv or ia into the oxyntic gland area of canine stomach caused a dose-dependent increase in the GBF, MBF and GVO2, PGE2 and LTC4 contents in the ethanol-treated gastric mucosa showed a 5-12 fold increase over the values in the intact mucosa. The generation of LTC4, but not PGE2, was significantly diminished by solcoseryl. Pre-treatment with indomethacin completely prevented the effects of solcoseryl on mucosal PGE2, but not LTC4 levels, and significantly reduced its circulatory and metabolic actions on the stomach. The results of these studies indicate that solcoseryl causes dilatation of gastric arterioles and precapillary sphincters thereby improving mucosal blood flow and oxygen supply. The results also suggest that endogenous prostaglandins serve as mediators of the vascular and possibly metabolic effects of the drug on the stomach. The observed reduction by solcoseryl in gastric biosynthesis of LTC4 during mucosal injury may be an important factor in the gastroprotective and anti-ulcer effects of solcoseryl.