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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rats subjected to ammonium chloride-induced metabolic acidosis or respiratory acidosis caused by hypercapnia were given alkalinization therapy with either sodium bicarbonate or Carbicarb. Ammonium chloride induced dose-dependent systemic acidosis but did not affect intracellular brain pH. Hypercapnia caused dose-dependent systemic acidosis as well as decreases in intracellular brain pH. Sodium bicarbonate treatment resulted in systemic alkalinization and increases in arterial PCO2 in both acidosis models, but it caused intracellular brain acidification in rats with ammonium chloride acidosis. Carbicarb therapy resulted in systemic alkalinization without major changes in arterial PCO2 and intracellular brain alkalinization in both acidosis models. These data demonstrate that bicarbonate therapy of systemic acidosis may be associated with "paradoxical" intracellular brain acidosis, whereas Carbicarb causes both systemic and intracellular alkalinization under conditions of fixed ventilation.
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PMID:Brain pH responses to sodium bicarbonate and Carbicarb during systemic acidosis. 254 32

Bioelectric activity of CO2-sensitive, ventrolateral medullary neurons (VLN(CS)) in organotypic cultures from the obex level of newborn rats was tested during changes of the intracellular pH (pHi) measured in BCECF-AM loaded cultures. Hypercapnia (pCO2 80-100 mmHg) reduced pHi by 0.15 +/- 0.06 units and stimulated neuronal discharges. Replacement of CO2/HCO3- in the bath by HEPES (26 mM, pH 7.4) for 10 min acidified pHi (0.07 +/- 0.03 units) and also excited VLN(CS). Ammonium chloride (10 mM, 1 min) initially alkalized (0.1 +/- 0.04) and thereafter acidified pHi (0.06 +/- 0.03), while the extracellular pH was first acidified and then alkalized. This resulted in neuronal discharge which were first suppressed and then accelerated. The findings strongly suggest that intracellular rather than extracellular acidification activates CO2-sensitive neurons.
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PMID:CO2-sensitive medullary neurons: activation by intracellular acidification. 959 70