Transmucosal gastric potential difference (TGPD) was measured in the antrum and fundus of the stomach in two groups of rats submitted to hemorrhagic shock. In the first group the stomach contained 2 cm3 of 0.1 N HCl and in the second 2 cm3 of physiological saline. After the hemorrhage both antral and fundal TGPD diminished significantly in both groups. Antral TGPD dropped from –20 to –6 mV (p < 0.001) in the first group and from –22 to –12 mV (p < 0.01) in the second group; fundal TGPD dropped from –41 to –16 mV (p < 0.001) in the first group and from –40 to –17 mV (p < 0.05) in the second group. 20 min after reinfusion of blood extracted during the hemorrhage, both antral and fundal TGPD returned to normal values in the rats instilled with physiological saline, while in those treated with HCl TGPD values remained at levels significantly lower than the baseline values (in the antrum –10 mV, p < 0.001; in the fundus –25 mV, p < 0.02). Only those rats whose stomachs contained HCl developed ulcers, mainly located in the fundus of the stomach. These results suggest that the energy metabolism of the cells of the gastric mucosa undergoes constant alteration from the earliest stages of hemorrhagic shock. These alterations are greater in the fundus than in the antrum, a fact compatible with the greater incidence of ulcers in the fundus. It is probable that in the presence of HCl in the stomach, back-diffusion of H+ occurs, leading to the formation of ulcers, while the metabolic alterations occurring in the absence of acid proved to be reversible.

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