Aim: Influence of acute or chronic exposure of the stomach to dilute acetic acid was examined in rats.Methods: Rats were given acetic acid (0.1-1.0%) p.o. acutely or twice daily for 4 weeks, and subsequently the gastric potential difference (PD), mucosal blood flow (GMBF) or ulcerogenic response to HCl/etahnol were examined.
Results: Acute exposure of the rat stomach to dilute acetic acid for 10 min caused a concentrationdependent reduction of PD and increase of GMBF. The acetic acid given acutely also reduced the severity of HCl/ethanol-induced gastric lesions in a concentration-dependent manner. The protective effect of acetic acid was significantly attenuated by prior administration of indomethacin (5 mg/kg) but not by NG-nitro-L-arginine methyl ester (L-NAME) or sensory deafferentation, although the increased GMBF response was partially mitigated by either indomethacin, L-NAME or sensory deafferentation. The mucosal exposure to 1% acetic acid for 10 min significantly increased the luminal release of PGE2, and this response was completely inhibited by indomethacin but not by L-NAME. Likewise, a similar gastroprotection was observed when acetic acid was given repeatedly for 4 weeks before challenge with HCl/ethanol, the effect being also reversed in the presence of indomethacin. Citric acid even at 1% had no effect on both gastric PD, GMBF and HCl/ethanol-induced gastric damage, by either acute or chronic treatment.
Conclusion: These results suggest that dilute acetic acid such as vinegar acts as a mild irritant to the stomach, resulting in adaptive cytoprotection with an increase of GMBF, and the protective action is mainly brought about by endogenous prostaglandins while the latter is mediated, at least partly, by nitric oxide and sensory neurons, in addition to prostaglandins.

Keywords: Acetic Acid, Gastric Mucosa, adaptive cytoprotection ethanol damage, endogenous prostaglandins