Effect of luminal ethanol on epithelial resistances and cell volume in isolated Necturus gastric mucosa.

Ethanol is a well-established "barrier breaker" in gastric mucosa, but its effects at the cellular level remain to be elucidated. Isolated Necturus antral mucosa was exposed luminally to 5-15% (v/v) ethanol at pH 3.0. Apical, basolateral, shunt, and internal resistances in surface epithelium were measured using 2-D cable analysis. Cell volume changes were determined from tetramethylammonium-loaded surface cells. Low luminal ethanol (5%) decreased basolateral resistance, presumably by opening of K+ channels, since this decrease was partially inhibited by the K+ channel blocker, quinine. Low ethanol decreased also epithelial cell volume, which was opposed by quinine, suggesting that efflux of intracellular K+ underlies this shrinkage. High luminal ethanol (15%) markedly decreased shunt and apical cell membrane resistances, and partially closed gap junctions as judged from increased epithelial internal resistance. Opening of basolateral K+ channels with resultant epithelial cell shrinkage might be among the initial steps in ethanol induced gastric injury. The changes in intraepithelial resistances provoked by stronger ethanol probably reflect emerging structural epithelial damage.