Variations in Transmucosal Gastric Potential Difference during Hemorrhagic Shock in the Rat

Abstract

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.

Effect of Gastric Cold Irrigation on Stress Ulceration

“…In fact, in a previous experiment we demonstrated that GTPD always falls during hemorrhage, but it gradually returns to basal values after rein fusion of the shed blood if no anatomical damage of the mucosal barrier has occurred. On the contrary, the postreinfusion GTPD does not recover in the presence of anatomi cal mucosal lesions [12]. Therefore, the smaller difference between basal and final GTPD values in rats treated with cold gas tric infusion reflects less severe mucosal damage.…”

“…Since it is commonly accepted that mucosal isch emia plays an important role in the patho genesis of gastric stress lesions [6,8,12], cooling appears to have contrasting effects on the ischemic gastric mucosa. It is well known that cooling reduces the energetic re quirements of tissues, lessening the ischemic damage but, on the other hand, gastric cool ing reduces the mucosal blood flow, aggrav ating the gastric ischemia [5,9], Therefore it seems important to assess the overall effect of cold and warm gastric irrigation during hemorrhagic shock in rats by evaluating the degree of gastric ulceration and the behavior of gastric transmucosal potential difference (GTPD), which is a very sensitive index of anatomical and functional alterations of the gastric mucosa [1,10,12].…”

Transmucosal Potential Difference as an Index of Esophageal Mucosal Integrity

“…Since the active transport of sodi um is relatively fast compared with the passive diffusion of chloride ions, the net result is a greater number of posi tive charges on the serosal surface and a greater number of negative charges on the luminal surface. Further, since epithelial types inherently differ with respect to rate and type of ions transported and/or the magnitude and type of epithelial resistance to passive ion movements, each tis sue has its own characteristic PD [10], PD originates through an energy-requiring process and has been shown to decline when oxygen availability is reduced [11][12][13][14],…”

Simultaneous Measurement and Recording of Gastric Potential Difference and Intragastric pH in Man

“…The luminal surface of the gastric mucosa is electrically negative when compared with the serosal surface [1], There is a prominent lumen-negative transmucosal potential dif ference in the stomach (gastric potential dif ference, GPD) [2], Even if different ions are implicated in the generation of GPD, its principal source seems to be the active transport of chloride ions from the intracellular space against both concentration and electrochemical gradients [2,3], GPD originates through an energyrequiring process and has been shown to decline when oxygen availability is reduced [4][5][6][7][8].…”