Role of luminal alkalinization in repair process of ethanol-induced mucosal damage in rat stomach.

Changes in transmucosal potential difference (PD) and luminal pH after intragastric application of ethanol were simultaneously determined in stomachs of anesthetized rats. When the stomachs were exposed to 5-50% ethanol for 10 min, the PD was abruptly reduced and gradually returned to the basal levels, while the luminal pH gradually increased; these responses were concentration-dependent. The reduction of PD with 10% ethanol rapidly returned to the basal level without any changes in luminal pH. The PD after 50% ethanol gradually returned to the basal level in 3 hr, during which time luminal pH was kept at around 6. In cimetidine plus atropine-treated rats, considerably greater amounts of HCO3- were evident in the perfusate. The surface mucosal cells damaged by 50% ethanol recovered in parallel with the recovery of PD. When the stomach pH was maintained at a low level by an intravenous infusion of histamine or intragastric perfusion of 0.01 N HCl, the PD remained at a reduced level and the mucosal damage was aggravated. The perfusion of 0.01 N NaHCO3 kept the luminal pH at around 8-9, but it did not affect the recovery process of PD after 50% ethanol. These results suggest that application of ethanol induces luminal alkalinization, probably by HCO3- diffusion through the broken barrier, which in turn plays a role in the recovery from damage.