Effects of prostaglandin E₁, E₂ and 16,16‐dimethyl‐E₂ on gastric mucosal microcirculation and basal acid output in the rat*

Abstract

The effects of prostaglandins E1 (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 micrograms ml-1), PGE2 (5 or 50 micrograms ml-1) or 16,16-dm-PGE2 (0.005, 0.05 or 0.5 microgram ml-1) increased VRBC dose-dependently without altering acid output, except for the highest dose of PGE2 (50 micrograms ml-1) which inhibited acid output. The latter occurred in spite of a seven- to eight-fold increase in VRBC. 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 micrograms kg-1 min-1) or 16,16-dm-PGE2 (0.02 microgram kg-1 min-1) caused an initial and transient (5-10 min) fall in systemic arterial blood pressure and a decrease in VRBC and acid output. Intravenous 16,16-dm-PGE2 in a dose which did not affect secretion or systemic arterial blood pressure (0.002 microgram kg-1 min-1) still significantly reduced VRBC. Thus, topically applied PGE1, PGE2 or 16,16-dm-PGE2 dose-dependently increase VRBC while intravenous administration of the same prostaglandins reduce VRBC.