Brain Carbonic Acid Acidosis after Acetazolamide
Abstract In cats in barbiturate anesthesia extracellular pH and potassium were continuously recorded from brain cortex by implanted microelectrodes. Implantation of the electrodes preserved the low permeability of the blood‐brain‐barrier to HCO 3 and H + ions as indicated by the development of brain...
| Published in: | Acta Physiologica Scandinavica |
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| Main Authors: | , , , |
| Format: | Article in Journal/Newspaper |
| Language: | English |
| Published: |
Wiley
1975
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| Subjects: | |
| Online Access: | http://dx.doi.org/10.1111/j.1748-1716.1975.tb05827.x https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fj.1748-1716.1975.tb05827.x https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1748-1716.1975.tb05827.x |
| Summary: | Abstract In cats in barbiturate anesthesia extracellular pH and potassium were continuously recorded from brain cortex by implanted microelectrodes. Implantation of the electrodes preserved the low permeability of the blood‐brain‐barrier to HCO 3 and H + ions as indicated by the development of brain acidosis by i.v. injection of HCO 3 . Acetazolamide (25 mg/kg) i.v. was followed by a marked brain acidosis which after 10 min had progressed to a drop in pH of 0.203 ± 0.046 (x ± S.D., n = 8). The slowness of the development of acidosis points to a direct effect of the carbonic anhydrase inhibition on the brain tissue. As a further support for this conclusion was considered the finding of a prolonged responsetime of brain pH to HCO 3 i.v., to CO 2 inhalation, and to hyperventilation after the acetazolamide inhibition. No changes in brain extracellular potassium were found. |
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