Gastric mucosal high-energy phosphate metabolism. Influence of ethanol and PGE2.

This study investigated potential alterations in gastric mucosal energy metabolism following exposure to the damaging agent 50% ethanol (50% EtOH) alone and after pretreatment with either 16,16-dimethyl (dmPGE2) or the mild irritant 25% ethanol (25% EtOH). Fasted rats (n = 12-26/group) were orally given 1 ml of normal saline (NS), dmPGE2 in a dose of 5 micrograms/kg, or 25% EtOH. Fifteen minutes later, they randomly received 1 ml of NS or 50% EtOH. After 5 min, rats were anesthetized and their stomachs rapidly excised, frozen in liquid nitrogen, and lyophyllized. Once dried, the surface area (in square millimeters) of mucosal lesions was quantitated. Mucosa was then scraped off the underlying muscularis. Tissue metabolites (ATP, ADP, AMP, lactate, pyruvate, glucose, and glucose-6-phosphate) were measured in deproteinized, neutralized samples by enzymatic methods. In conjunction with the development of mucosal lesions involving an average of 45 mm2, ATP was significantly (P < 0.05) lower and AMP significantly higher in 50% EtOH-treated animals (indicating dephosphorylation) when compared with NS controls. Although both 25% EtOH and dmPGE2 prevented these lesions, only 25% EtOH prevented the ATP and AMP alterations. Fifty percent EtOH also significantly increased the tissue content of glucose and lactate over control values while glucose-6-phosphate was significantly decreased. With both protective agents pyruvate levels were significantly reduced, while glucose and lactate levels were not affected. In contrast to dmPGE2, the mild irritant (25% EtOH) significantly increased glucose-6-phosphate levels over control.(ABSTRACT TRUNCATED AT 250 WORDS)