Abstract
Summary
Prolonged administration of acetazoleamide to alligators leads to the excretion of considerable amounts of chloride which produces an alkalemia. A continued K excretion also occurs which has little effect on the plasma level, presumably due to a removal of K from the cells in an effort to compensate for the loss. No evidence of the development of a refractory state to acetazoleamide after 30 days of injections was noted nor was there any sign that the decreased plasma Cl prevented the excretion of Cl. The degree of K loss was not directly correlated with hydrogen ion excretion. Two new carbonic anhydrase inhibitors, chlorothiazide and dichlorphenamide were tested. Dichlorphenamide was more active in promoting K and Cl loss at low dose levels than acetazoleamide. Chlorothiazide showed no significant activity. Since the effects noted after the inhibition of carbonic anhydrase by acetazoleamide and dichlorphenamide are not the same, it is probable that something more than simple inhibition is involved.
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