| Literature DB >> 7012 |
Abstract
In respiratory alkalosis the fall in CSF bicarbonate is in part due to increased CSF lactate. The rest of CSF HCO3 fall may be actively regulated or as more recent evidence suggests is dependent on plasma HCO3 fall. Therefore, the relationship between plasma and CSF HCO3 changes was studied during 4 hours of respiratory alkalosis (PaCO2=20 mm Hg) in anesthetized dogs when plasma HCO3: (1) fell normally, (2) kept 'normal' by NaHCO3 infusion, (3) increased by infusing more NaHCO3, and (4) reduced by infusing HCl. In respiratory alkalosis plasma and CSF HCO3 fell 4.6 and 3.8 mEQ/L, respectively. In hypocapnia and 'normal' plasma HCO3 CSF HCO3 fell 2 mEq/L and lactate increased 1.33 mEq/L. In hypocapnia and metabolic alkalosis plasma HCO3 increased 6.5 mEq/L and CSF HCO3 remained unchanged and lactate increased 2.12 mEq/L. In combined hypocapnia and metabolic acidosis plasma HCO3 fall 10.5 mEq/L but CSF HCO3 fell 3.1 mEq/L and CSF pH returned to normal at 4 hours. Therefore CSF HCO3 fall in hypocapnia is primarily and critically dependent on the simultaneous fall in plasma HCO3 content, with a minimal contribution from CNS lactate increase. When CSF PH has returned to normal, however, CSF HCO3 fall is stopped despite further falls in plasma HCO3.Entities:
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Year: 1976 PMID: 7012 DOI: 10.1016/0034-5687(76)90104-3
Source DB: PubMed Journal: Respir Physiol ISSN: 0034-5687