Cheung L Y, Porterfield G
Am J Surg. 1979 Jan;137(1):106-10. doi: 10.1016/0002-9610(79)90019-9.
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+.
在犬离体模型中评估了静脉输注碳酸氢钠对牛磺胆酸钠局部应用和失血性休克所致胃黏膜损伤的影响。正如预期的那样,胃黏膜暴露于牛磺胆酸钠和酸会导致氢离子(H+)过度反向扩散和轻度黏膜损伤。在对照犬中,失血性休克会加重这种黏膜损伤。接受静脉输注碳酸氢钠的试验犬的黏膜损伤程度明显较轻。静脉输注碳酸氢钠提供的保护作用并非由于进入组织的H+量减少,因为对照犬和试验犬管腔内的净H+损失没有显著差异。静脉输注碳酸氢钠的保护作用可能继发于黏膜对H+耐受性的增强。这些结果支持这样一种假说,即失血性休克期间黏膜损伤的加重可能是胃黏膜缓冲流入H+能力下降的结果。