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Publication : Respiratory acidosis in carbonic anhydrase II-deficient mice.

First Author  Lien YH Year  1998
Journal  Am J Physiol Volume  274
Issue  2 Pt 1 Pages  L301-4
PubMed ID  9486217 Mgi Jnum  J:46053
Mgi Id  MGI:1197036 Doi  10.1152/ajplung.1998.274.2.L301
Citation  Lien YH, et al. (1998) Respiratory acidosis in carbonic anhydrase II-deficient mice. Am J Physiol 274(2 Pt 1):L301-4
abstractText  To investigate the role of carbonic anhydrase (CA) II on pulmonary CO2 exchange, we analyzed arterial blood gases from CA II-deficient and normal 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) and a high Pco2 (47.4 +/- 5.3 mmHg), consistent with mixed respiratory and metabolic acidosis. To eliminate the influence of metabolic acidosis 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 Pco2 and [HCO3-]. The metabolic acidosis in CA II-deficient mice was corrected ([HCO3-], 22.9 +/- 2.4 meq/l), and respiratory acidosis became more profound (Pco2, 50.4 +/- 2.4 mmHg). These results indicate that CA II-deficient mice have a partial respiratory compensation for metabolic acidosis. We conclude that CA II-deficient mice have a mixed respiratory and metabolic acidosis. It is most likely that CO2 retention in these animals is due to CA II deficiency in both red blood cells and type II pneumocytes.
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