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 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.
Lien
Y H
YH
Department of Medicine, University of Arizona Health Sciences Center, Tucson 85724, USA.
Lai
L W
LW
D000142:Acidosis, Respiratory / Q000201:enzymology*; D000818:Animals; D001784:Blood Gas Analysis; D015153:Blotting, Western; D002256:Carbonic Anhydrases / Q000172:deficiency / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D012129:Respiratory Function Tests
D002256:Carbonic Anhydrases