Effects of prostaglandin E1, E2and 16,16‐dimethyl‐E2on gastric mucosal microcirculation and basal acid output in the rat*

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Abstract
The effects of prostaglandins E, (PGE1), E2(PGE2) and 16, 16‐dimethyl‐E2(16, 16‐dm‐PGE2) on the gastric mucosal microcirculation and (spontaneous) acid output were studied in anaesthetized rats. The superficial mucosal vessels were monitored on a TV screen using a microscope, TV camera and videorecorder for off‐line analysis of red cell velocities (VRBC) and vessel diameters, from which the blood flow (QRBC) was calculated. The prostaglandins were either applied topically to the solution bathing the exposed mucosa or administered intravenously as a continuous infusion. Topical application of PGE1(0.5 or 5 μgml‐1), PGE2(5 or 50 μg ml‐1) or 16, 16‐dm‐PGE2(0.005, 0.05 or 0.5 μg ml‐1) increasedVRBCdose‐dependently without altering acid output, except for the highest dose of PGE2(50 μg ml‐1) which inhibited acid output. The latter occurred in spite of a seven‐to eight‐fold increase inVRBC. Mucus secretion (evidenced by an impaired resolution of the TV image) also increased during topical application of the prostaglandins especially at higher doses. Intravenous PGE1, PGE2(2.0 μg kg‐1min_1) or 16, 16‐dm‐PGE2(0.02 μg kg‐1min_1) caused an initial and transient (5–10 min) fall in systemic arterial blood pressure and a decrease inVRBCand acid output. Intravenous 16, 16‐dm‐PGE2in a dose which did not affect secretion or systemic arterial blood pressure (0.002 μg kg‐1min‐1) still significantly reducedVRBC. Thus, topically applied PGE1, PGE2or 16, 16‐dm‐PGE2dose‐dependently increaseVRBCwhile intravenous administration of the same prostaglandins reduceVRBC.