RESPIRATORY-ACIDOSIS IN CARBONIC-ANHYDRASE II-DEFICIENT MICE

To investigate the role of carbonic anhydrase (CA) II on pulmonary CO2 exchange, we analyzed arterial blood gases from CA II-deficient and n ormal control mice. CA II-deficient mice had a low arterial blood pH ( 7.18 +/- 0.06) and HCO3- concentration ([HCO3-]; 17.5 +/- 1.9 meq/l) a nd a high Pco(2) (47.4 +/- 5.3 mmHg), consistent with mixed respirator y and metabolic acidosis. To eliminate the influence of metabolic acid osis on arterial blood gases, NaHCO3 (4 mmol/kg body weight) was given intraperitoneally, and arterial blood gases were analyzed 4 h later. Normal mice had a small increase in pH and were able to maintain Pco(2 ) and [HCO3-]. The metabolic acidosis in CA II-deficient mice was corr ected ([HCO3-], 22.9 +/- 2.4 meq/l), and respiratory acidosis became m ore profound (Pco(2), 50.4 +/- 2.4 mmHg). These results indicate that CA II-deficient mice have a partial respiratory compensation for metab olic acidosis. We conclude that CA II-deficient mice have a mixed resp iratory and metabolic acidosis. It is most likely that CO2 retention i n these animals is due to CA II deficiency in both red blood cells and type II pneumocytes.