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Lithium chloride (LiCl) has been shown to decrease gastric acid secretion and protect against ethanol-induced hemorrhagic gastritis in the rat. To further investigate these properties, two sets of experiments were performed in dogs with chronic Heidenhain pouches to study the effect of LiCl on histamine-stimulated gastric acid secretion and bile-induced disruption of the gastric mucosal barrier. In the first experiments the effect of LiCl on intravenous histamine-stimulated gastric secretion (40 micrograms/kg . hr) was determined. LiCl (30 mg/kg . hr) significantly reduced gastric acid secretion when compared to normal saline control (457 +/- 87 mueq H+/10 min versus 637 +/- 112 mueq H+/10 min, P less than 0.05). Serum and gastric lithium levels were determined and a significant inverse linear correlation existed between acid output and serum and gastric lithium levels. In the second set of experiments the effect of LiCl on bile-induced disruption of the gastric mucosal barrier was determined. Heidenhain pouches were continuously perfused with a pH 2 acid test solution and indices of mucosal barrier function (net acid back-diffusion and potential difference) were determined. LiCl (30 mg/kg . hr) significantly reduced both the increase in acid-back diffusion and the fall in potential difference with bile injury (5 mM taurodeoxycholate). In conclusion, these studies indicate that LiCl (1) decreases histamine-stimulated gastric acid secretion, and (2) diminishes bile-induced disruption of the gastric mucosal barrier in the canine Heidenhain pouch.
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