Effect of 16, 16-dimethyl PGE2 on resting and histamine-stimulated gastric mucosal blood flow.

Using [14C]aminopyrine clearance as a measure of mucosal blood flow, 16,16-dimethyl PGE2 was administered orally as a single bolus and its effects on resting and histamine-stimulated gastricmucosal blood flow assessed in conscious dogs with vagally denervated gastric pouches. No effect on resting mucosal flow was observed with any of the doses (ie, 2, 10, and 50 microgram/kg) of prostaglandin given. In histamine-stimulated experiments, intravenous infusion of histamine dihydrochloride (1 mg/hr) elicited a significant (P < 0.0005) increase from basal in gastric acid production, volume output, and gastric mucosal blood flow which remained unchanged for the duration of the study. Prostaglandin (50 microgram/kg) significantly decreased (P < 0.0005) these secretory responses and markedly inhibited (P < 0.005) mucosal blood flow without altering the ratio (R) of flow to the volume rate of secretion. The observation that R was unchanged suggests that this inhibitory action of 16,16-dimethyl PGE2 on gastric secretion and blood flow was mediated through direct effects on gastric parietal cells rather than any primary alteration in the gastric microcirculation. We conclude that 16,16-dimethyl PGE2 given orally has no effect on the resting gastric mucosal circulation and that any reduction in mucosal flow during histamine stimulation is secondary to its inhibitory effects on gastric acid secretion.