Dual contribution theory of regulation of CSF HCO3 in respiratory acidosis.
Regulation of CSF HCO3-in respiratory acidosis was studied in light of the "dual contribution theory," which proposed that there were two sources for the CSF HCO3-increase: 1) HCO3-by diffusion from plasma and 2) HCO3-generated in the CNS and catalyzed by the local carbonic anhydrase (J. Appl. Physiol. 38: 504-512, 1975). In anesthetized dogs with an increase in Paco2 of 30 mmHg for 4 h the plasma HCO3 increased 2 meq/1 and CSF 6 meq/1. In combined respiratory and metabolic acidosis, plasma HCO3-did not increase but CSF HCO3-increased 6 meq/1. In combined acidosis and intraventricular injections of acetazolamide no increase in plasma or CSF HCO3-occurred. In combined respiratory acidosis and metabolic alkalosis and intraventricular acetazolamide, plasma HCO3-increased 15 meq/1 but CSF HCO3-increased 6 meq/1. Brain and CSF ammonia increased linearly and selectively with the increase in the relative contribution of CNS HCO3-increase. Therefore regulation of CSF HCO3-in respiratory acidosis depends on both components of the dual contribution theory, where each component can provide the total CSF HCO3-increase under appropriate experimental conditions. The control mechanism may be sensitive to changes in [H+] on the brain side of the blood-brain barrier.
D000136:Acid-Base Equilibrium; D000142:Acidosis, Respiratory / Q000134:cerebrospinal fluid*; D000641:Ammonia / Q000378:metabolism; D000818:Animals; D001639:Bicarbonates / Q000097:blood / Q000134:cerebrospinal fluid*; D001921:Brain / Q000378:metabolism; D002245:Carbon Dioxide / Q000097:blood / Q000134:cerebrospinal fluid; D002256:Carbonic Anhydrases / Q000378:metabolism; D002555:Cerebrospinal Fluid / Q000201:enzymology; D004285:Dogs; D006863:Hydrogen-Ion Concentration
D001639:Bicarbonates; D002245:Carbon Dioxide; D000641:Ammonia; D002256:Carbonic Anhydrases