Lithium chloride reduced the measured parameters of gastric secretion (gastric volume, hydrogen ion concentration, and gastric acid output) 2 h after intracerebroventricular, intravenous, or subcutaneous administration in pylorus-ligated rats, in a dose-dependent manner. Intracerebroventricular administration of lithium was approximately five times and 10 times more potent than intravenous and subcutaneous injection, respectively. Timecourse study demonstrated that the action of lithium (400 μg) on gastric secretion reached a peak at 1 h after intracerebroventricular administration; however, the effects on volume and output were still significant after 8 h. Prior intracerebroventricular injection of indomethacin (400 μg) reversed the action of centrally administered lithium on gastric secretion. However, central administration of the opiate receptor blocker naltrexone (100 μg), as well as subcutaneous administration of indomethacin (5 mg/kg), failed to modify the effect of lithium on gastric acid secretion. Our data suggest that lithium appears to act centrally to modulate gastric acid secretion in rats through a mechanism involving the synthesis of prostaglandinlike material(s) in the brain. Furthermore, the effect of centrally administered lithium is independent of stimulation of opiate receptor(s) in the brain.
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