Respiratory acidosis in carbonic anhydrase II-deficient mice

• Published in: American journal of physiology. Lung cellular and molecular physiology 1998-02, Vol.274 (2), p.301-L304
• Main Authors: Lien, Yeong-Hau H, Lai, Li-Wen
• Format: Article
• Language: English
• ISSN: 1040-0605; 1522-1504
• DOI: 10.1152/ajplung.1998.274.2.l301

Department of Medicine, University of Arizona Health Sciences Center, Tucson, Arizona 85724 To investigate the role of carbonic anhydrase (CA) II on pulmonary CO 2 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 concentration ([ ]; 17.5 ± 1.9 meq/l) and a high P CO 2 (47.4 ± 5.3 mmHg), consistent with mixed respiratory and metabolic acidosis. To eliminate the influence of metabolic acidosis on arterial blood gases, NaHCO 3 (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 P CO 2 and [ ]. The metabolic acidosis in CA II-deficient mice was corrected ([ ], 22.9 ± 2.4 meq/l), and respiratory acidosis became more profound (P CO 2 , 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 CO 2 retention in these animals is due to CA II deficiency in both red blood cells and type II pneumocytes. carbon dioxide exchange; arterial blood gas; metabolic acidosis; lung