Effect of acetazolamide on rat gastric mucosal protection and stimulated bicarbonate secretion with 16,16-dimethyl PGE2.
The effect of pretreatment with acetazolamide, a carbonic anhydrase inhibitor, was studied on the mucosal protection provided by and the gastric alkaline secretion stimulated by 16,16-dimethyl prostaglandin E2. Using a model employing a chamber of the rat whole stomach, 16,16-dimethyl prostaglandin E2 (1 microgram/ml) was found to significantly (p less than 0.05) increase the secretion of bicarbonate by 31.1 +/- 4.1 mu Eq/hr over basal values. This stimulated secretion was inhibited (to 18.0 +/- 2.2 mu Eq/hr) by pretreatment with acetazolamide (50 mg/kg body weight). In a separate series of experiments, the ability of this concentration of 16,16-dimethyl prostaglandin E2 to protect the rat stomach from necrosis caused by absolute ethanol was not impaired by prior exposure to the same dose of acetazolamide.
D015064:16,16-Dimethylprostaglandin E2 / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D000086:Acetazolamide / Q000494:pharmacology*; D000818:Animals; D001639:Bicarbonates / Q000378:metabolism*; D000431:Ethanol / Q000037:antagonists & inhibitors; D005753:Gastric Mucosa / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D006863:Hydrogen-Ion Concentration; D008297:Male; D009336:Necrosis; D011459:Prostaglandins E, Synthetic / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D013268:Stimulation, Chemical
D001639:Bicarbonates; D011459:Prostaglandins E, Synthetic; D000431:Ethanol; D015064:16,16-Dimethylprostaglandin E2; D000086:Acetazolamide