UNLABELLED: This study examined the role of the gastric mucosal blood flow (MBF) in the gastric cytoprotection produced by prostacyclin (PGI2) and prostaglandin E2 (PGE2) in dogs. An acidified solution of saline was applied topically on the canine gastric mucosa with and without ethanol at various concentrations. Ethanol applied to the mucosa of a stomach flap preparation, in concentrations ranging from 5 to 80%, gradually decreased the transmucosal potential difference (PD) from -58 to -5 mV and increased net ionic fluxes. MBF gradually increased at lower concentrations of ethanol, reaching the peak of about 50% above basal at 20% ethanol and then declining at 40 and 80% ethanol. PGI2 (10 micrograms/kg/h) prevented the changes in PD and ion fluxes produced by lower but not higher concentrations of ethanol and this was accompanied by a marked increase in the MBF above the level produced by ethanol alone. The instillation of acidified 15% ethanol into Heidenhain pouch (HP) reduced the PD from -57 to -40 mV and elicited large net H+ and Na+ fluxes. MBF was increased by 30%. PGI2 (10 micrograms/kg/h) completely prevented ethanol-induced changes in PD, reduced ionic fluxes, and raised the MBF twofold. On the contrary PGE2 (80 micrograms/kg/h) did not affect ethanol-induced alterations in PD, ion fluxes, and MBF. CONCLUSIONS: PGI2, but not PGE2, effectively protects the canine gastric mucosa against the damage produced by ethanol. This cytoprotection may be due to increased mucosal circulation, which by an unknown mechanism interferes with the mucosal damage caused by ethanol.
UNLABELLED: This study examined the role of the gastric mucosal blood flow (MBF) in the gastric cytoprotection produced by prostacyclin (PGI2) and prostaglandin E2 (PGE2) in dogs. An acidified solution of saline was applied topically on the canine gastric mucosa with and without ethanol at various concentrations. Ethanol applied to the mucosa of a stomach flap preparation, in concentrations ranging from 5 to 80%, gradually decreased the transmucosal potential difference (PD) from -58 to -5 mV and increased net ionic fluxes. MBF gradually increased at lower concentrations of ethanol, reaching the peak of about 50% above basal at 20% ethanol and then declining at 40 and 80% ethanol. PGI2 (10 micrograms/kg/h) prevented the changes in PD and ion fluxes produced by lower but not higher concentrations of ethanol and this was accompanied by a marked increase in the MBF above the level produced by ethanol alone. The instillation of acidified 15% ethanol into Heidenhain pouch (HP) reduced the PD from -57 to -40 mV and elicited large net H+ and Na+ fluxes. MBF was increased by 30%. PGI2 (10 micrograms/kg/h) completely prevented ethanol-induced changes in PD, reduced ionic fluxes, and raised the MBF twofold. On the contrary PGE2 (80 micrograms/kg/h) did not affect ethanol-induced alterations in PD, ion fluxes, and MBF. CONCLUSIONS:PGI2, but not PGE2, effectively protects the canine gastric mucosa against the damage produced by ethanol. This cytoprotection may be due to increased mucosal circulation, which by an unknown mechanism interferes with the mucosal damage caused by ethanol.