Abstract
Summary
Intraarterial infusion of PGI2 or PGE2 causes a dose-dependent inhibition of histamine-stimulated gastric acid secretion in an in vivo-chambered stomach, PGI2 being less potent inhibitor than PGE2. While PGE2 decreases gastric mucosal blood flow, PGI2 causes a marked and dose-dependent increase in mucosal blood flow. PGI2 is also secretory inhibitor after intravenous, but not after intraportal administration. 6-Keto-PGF1α, a breakdown product of PGI2, has no effect on gastric secretion or gastric mucosal circulation. PGI2 lowers systemic arterial blood pressure, the effect being more pronounced after intravenous than intraarterial or portal administration. This suggests a marked in-activation of this PG during the liver transit.
This work was supported by Research Grant 10-RMZ-1.
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