The CSF HCO3 increase in hypercapnia relationshp to HCO3, glutamate, glutamine and NH3 in brain.
To study the role of carbonic anhydrase in the CSF [HCO3] increase in respiratory acidosis and its effect on brain ammonia, anesthetized rats were subjected to hypercapnia (7% CO2) for 2 hours. The animals received periodic intraventricular injections of either 'mock' CSF or 'mock' CSF and acetazolamide for 45 minutes prior and during hypercapnia when: (a) plasma [HCO3-] was allowed to increase normally and (2) plasma [HCO3] increase was prevented by i.v. HC1 infusion, CSF [HCO3] increased 8.5 mM/L after 2 hours of hypercapnia (delta PCO2 40) in the rats with intraventricular 'mock' CSF injections, and only 6 mM/L in the animals with acetazolamide injections. CSF [HCO3-] increased 7 mM/L during hypercapnia and HCl infusion with intraventricular 'mock' CSF injections, but only 2 mM/L with acetazolamide injections. Changes in total brain CO2 (increase) and brain glutamic acid (decrease) in hypercapnia were not affected by intraventricular acetazolamide and i.v. HCl. The increase of brain NH4+ and glutamine in hypercapnia was reduced in these conditions. It is concluded that there are at least two sources for the CSF [HCO3-] increase in hypercapnia; one formed in the CNS and dependent on carbonic anhydrase, and the other derived from plasma [HCO3-] increase.
D000086:Acetazolamide / Q000494:pharmacology; D000641:Ammonia / Q000378:metabolism; D000818:Animals; D001639:Bicarbonates / Q000134:cerebrospinal fluid / Q000378:metabolism*; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D002555:Cerebrospinal Fluid; D005971:Glutamates / Q000378:metabolism; D005973:Glutamine / Q000378:metabolism; D006851:Hydrochloric Acid / Q000494:pharmacology; D006863:Hydrogen-Ion Concentration; D006935:Hypercapnia / Q000134:cerebrospinal fluid / Q000378:metabolism*; D008297:Male; D051381:Rats
D001639:Bicarbonates; D005971:Glutamates; D005973:Glutamine; D000641:Ammonia; D000086:Acetazolamide; D006851:Hydrochloric Acid