Regulation of pH and HCO3 in brain and CSF of the developing mammalian central nervous system.
Acute (2-h) metabolic acidosis or alkalosis was induced in immature rats to ascertain the ability of their incompletely-developed CNS to regulate pH when challenged with perturbations in blood [H] and [HCO3]. Brain and cisternal CSF pH were determined from steady-state distribution of [14C]dimethadione, a weak organic acid. By 1 week post partum, there was a remarkable stability of pH in the cerebral cortex of animals subjected to arterial pH extremes of 7.1 and 7.5. However, CSF pH in 1-week-old animals rendered alkalotic remained 0.07-0.08 units above control due to lack of a compensatory increase in pCO2, and to a blood-CSF barrier apparently more permeable to HCO3. As arterial HCO3, i.e. [HCO3]art, was varied from about 10 to 30 mmol/l, the infants maintained [HCO3]csf only half as effectively as adults, i.e. delta [HCO3]art was 0.4 and 0.2 at 1 and greater than 4 weeks, respectively. Throughout postnatal ontogenesis, [HCO3]csf was more resistant to alteration by metabolic acidosis than by alkalosis. Overall, the results indicate that immature rats challenged with systemic acid-base loads are less capable than adults in regulating CSF pH, but they are able to maintain brain pH.
D000138:Acidosis / Q000134:cerebrospinal fluid / Q000378:metabolism*; D000375:Aging / Q000378:metabolism*; D000471:Alkalosis / Q000134:cerebrospinal fluid / Q000378:metabolism*; D000818:Animals; D001639:Bicarbonates / Q000134:cerebrospinal fluid / Q000378:metabolism; D001921:Brain / Q000254:growth & development / Q000378:metabolism*; D002245:Carbon Dioxide / Q000134:cerebrospinal fluid / Q000378:metabolism; D004114:Dimethadione / Q000134:cerebrospinal fluid / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D051381:Rats; D011919:Rats, Inbred Strains
D001639:Bicarbonates; D002245:Carbon Dioxide; D004114:Dimethadione