Respiratory acidosis in carbonic anhydrase II-deficient mice

Yeong Hau H Lien, Li-Wen Lai

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume274
Issue number2 18-2
StatePublished - 1998

Fingerprint

Carbonic Anhydrase II
Respiratory Acidosis
Acidosis
Gases
Alveolar Epithelial Cells
Erythrocytes
Body Weight
Lung

Keywords

  • Arterial blood gas
  • Carbon dioxide exchange
  • Lung
  • Metabolic acidosis

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Cell Biology
  • Physiology
  • Physiology (medical)

Cite this

Respiratory acidosis in carbonic anhydrase II-deficient mice. / Lien, Yeong Hau H; Lai, Li-Wen.

In: American Journal of Physiology - Lung Cellular and Molecular Physiology, Vol. 274, No. 2 18-2, 1998.

Research output: Contribution to journalArticle

@article{b940e357376945d28e591c32eaee77d3,
title = "Respiratory acidosis in carbonic anhydrase II-deficient mice",
abstract = "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.",
keywords = "Arterial blood gas, Carbon dioxide exchange, Lung, Metabolic acidosis",
author = "Lien, {Yeong Hau H} and Li-Wen Lai",
year = "1998",
language = "English (US)",
volume = "274",
journal = "American Journal of Physiology",
issn = "0363-6143",
publisher = "American Physiological Society",
number = "2 18-2",

}

TY - JOUR

T1 - Respiratory acidosis in carbonic anhydrase II-deficient mice

AU - Lien, Yeong Hau H

AU - Lai, Li-Wen

PY - 1998

Y1 - 1998

N2 - 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.

AB - 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.

KW - Arterial blood gas

KW - Carbon dioxide exchange

KW - Lung

KW - Metabolic acidosis

UR - http://www.scopus.com/inward/record.url?scp=0031932913&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031932913&partnerID=8YFLogxK

M3 - Article

VL - 274

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0363-6143

IS - 2 18-2

ER -