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

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Abstract
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.