Substituted thiadiazolines as inhibitors of central nervous system carbonic anhydrase

1975 ◽  
Vol 18 (4) ◽  
pp. 351-354 ◽  
Author(s):  
James J. Lukes ◽  
Karl A. Nieforth
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Carbonic Anhydrase

Effects of acetazolamide on cerebrospinal fluid ions in metabolic alkalosis in dogs

1987 ◽  
Vol 62 (4) ◽  
pp. 1582-1588 ◽  
Author(s):  
S. Javaheri
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Carbonic Anhydrase ◽  
Metabolic Alkalosis ◽  
Renal Effects ◽  
Mechanically Ventilated ◽  
Group I ◽  
The Central Nervous System ◽  
Group Ii

We hypothesized that inhibition of carbonic anhydrase in the central nervous system by acetazolamide should limit the rise in cisternal cerebrospinal fluid (CSF) [HCO3-] observed in metabolic alkalosis. To test this hypothesis, isosmotic isonatremic metabolic alkalosis was produced in two groups of anesthetized, paralyzed, and mechanically ventilated dogs (8 in each group). Group II animals received 50 mg/kg of acetazolamide intravenously 1 h before induction of metabolic alkalosis of 5-h duration. Renal effects of acetazolamide were eliminated by ligation of renal pedicles. In both groups cisternal CSF [Na+] remained relatively constant during metabolic alkalosis. In group I CSF [Cl-] decreased 3.6 and 8.2 meq/l, respectively, 2.5 and 5 h after induction of metabolic alkalosis. Respective increments in CSF [HCO3-] were 3.4 and 6.0 meq/l. In acetazolamide-treated dogs, during metabolic alkalosis, increments in CSF [HCO3-] (4.8 and 7.2 meq/l, respectively, at 2.5 and 5 h) and decrements in CSF [Cl-] (9.1 and 13.3 meq/l) were greater than those observed in group I. We conclude that, in dogs with metabolic alkalosis and bilateral ligation of renal pedicles, acetazolamide impairs CSF regulation of HCO3- and Cl- ions; acetazolamide not only failed to impede HCO3- rise but actually appeared to increase it. The mechanisms for these observations are discussed.

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