Ventilatory response to carbonic anhydrase inhibition in cats: effects of acetazolamide in intact vs peripherally chemodenervated animals.

Hyperventilation induced by red cell carbonic anhydrase inhibition (CAI) has been observed frequently; its mechanism, however, is still obscure. In the present study in anaesthetized cats, we have investigated the effect of 50 mg/kg acetazolamide, a carbonic anhydrase inhibitor, on ventilation. In order to determine the role of the peripheral chemoreceptors, we compared the response in peripherally chemodenervated and intact cats. Furthermore, in cats with intact peripheral chemoreceptors, we determined hypoxic sensitivity before and 2 h after i.v. infusion of the drug. In all animals, acetazolamide caused a large increase in ventilation. However, the peripherally chemodenervated animals developed a significantly larger response than the intact animals (respectively about 200 and 100% increases in ventilation). The first group also showed a significantly larger fall in PACO2. In the intact animals studied, acetazolamide virtually abolished the hypoxic sensitivity which existed before infusion of the drug. We conclude that acetazolamide, at the dose studied, causes a decrease in activity of the peripheral chemoreceptors, and also a decrease (c.q. removal) of their sensitivity to PaO2 changes. The increase in ventilation by acetazolamide is probably caused by an action of the drug on the central nervous system, possibly on the central chemoreceptors.