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Department of Medicine, University of Arizona Health Sciences Center, Tucson, Arizona 85724
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
concentration
([
]; 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
[
]. The metabolic
acidosis in CA II-deficient mice was corrected
([
], 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.
carbon dioxide exchange; arterial blood gas; metabolic acidosis; lung
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