Protection of gastric mucosa against acute ulceration by intravenous infusion of sodium bicarbonate.
The influence of intravenous infusion of sodium bicarbonate on gastric mucosal injury induced by topical sodium taurocholate and hemorrhagic shock was assessed in a canine ex vivo model. As expected, exposure of the gastric mucosa to sodium taurocholate and acid resulted in excessive back diffusion of hydrogen ions (H+) and mild mucosal damage. This mucosal injury was enhanced by hemorrhagic shock in the control dogs. The degree of mucosal injury was significantly less in the test dogs that received intravenous infusions of sodium bicarbonate. The protection afforded by intravenous bicarbonate was not due to a reduction in the amount of H+ entering the tissue, since the net H+ loss from the lumen was not significantly different between the control and the test dogs. The protection effect of intravenous infusion of sodium bicarbonate is probably secondary to an enhancement of mucosal tolerance to H+. These results support the hypothesis that the enhancement of mucosal injury during hemorrhagic shock may be a result of a decrease in the ability of the gastric mucosa to buffer the influxing H+.
D000818:Animals; D001639:Bicarbonates / Q000008:administration & dosage / Q000627:therapeutic use*; D001769:Blood; D004285:Dogs; D005753:Gastric Mucosa / Q000187:drug effects; D006863:Hydrogen-Ion Concentration; D007263:Infusions, Parenteral; D009336:Necrosis; D012771:Shock, Hemorrhagic / Q000150:complications*; D013276:Stomach Ulcer / Q000139:chemically induced / Q000209:etiology / Q000517:prevention & control*; D013656:Taurocholic Acid
D001639:Bicarbonates; D013656:Taurocholic Acid