Abstract
This study was conducted to examine the influence of acetazolamide and its noncarbonic anhydrase inhibitory analog, CL-13,850 (2-acetylamino-1,3,4,4-thiadiazole 5-( n-t-butyl) sulfonamide), on the hypothermic response and brain accumulation of chlorpromzine in the rat. The hypothermic response induced by 10 mg/kg chlorpromazine was both potentiated and prolonged after treatment with 50 mg/kg acetazolamide but not with the inactive analog. Two and one-half hours after chlorpromazine, the rectal temperatures in control animals were lowered 3.3°C vs. 4.90°C in acetazolamide-treated animals. After 9 hr, control animal temperatures were essentially back to normal, but treated animal temperatures were still 2.6°C below normal. The acetazolamide-potentiated hypothermia induced by chlorpromazine was accompanied by increased brain levels of chlorpromazine. The inactive analog did not modify the pharmacologic activity or brain level of chlorpromazine. The results demonstrate the potential pharmacologic and/or toxicologic significance of altered drug action following carbonic anhydrase inhibition.
Published Version
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