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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The intracellular pH (pHi) and bicarbonate concentration ([HCO3-]icw) of cardiac and skeletal muscles were monitored during respiratory alkalosis in order to further elucidate the homeostatic processes which operate in these tissues to ameliorate deviations from normal acid-base status. Rats were mechanically hyperventilated to induce hypocapnia, pHi was determined by the DMO method, and [HCO-3]icw was calculated from the Henderson-Hasselbalch equation using pHi and the partial pressure of carbon dioxide of vena caval blood. A significant intracellular alkalosis occurred in both cardiac and skeletal muscles during hypocapnia, but the changes in pHi were less in the heart than in skeletal muscle. The decreases in cardiac [HCO-3]icw were greater than those attributable to the physicochemical buffering of the heart. These data are consistent with an intramyocardial source of protons other than physicochemical buffering during respiratory alkalosis. The decreases in skeletal muscle [HCO-3]icw were less than those due to physicochemical buffering. These data are consistent with a net extrusion from skeletal muscles cells of the protons derived from physicochemical buffering during respiratory alkalosis.
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PMID:The effects of hypocapnia on intracellular pH and bicarbonate. 642 99

Interregional differences in intracellular pH (pHi) in brain tissue, and its regulation following 1 and 5 h of respiratory alkalosis (with and without hypoxemia) were determined in N2O anesthetized dogs. Two techniques for pHi estimation were used (TCO2 and 14C-DMO) and included corrections for measured extracellular fluid (35SO4(2-)) space (ECS). Cortical pHi by the two techniques agreed closely in control and in 3 of the 4 experimental conditions, suggesting: (a) our estimation of extracellular fluid (ECF) [HCO3-] from measured CSF [HCO3-] was a valid assumption; and (b) our method had sufficient resolution to determine the magnitude of brain pHi regulation during respiratory acid-base disturbances. When moderate normoxic respiratory alkalosis (PaCO2 approximately 25 mm Hg) was imposed for 5 h, pHi (in most brain regions) was well regulated and always exceeded the incomplete regulation noted in bulk CSF. When moderate hypoxemia (PaO2 approximately 45 mm Hg) accompanied hypocapnia, pHi was more closely regulated during the early phase (1 h) of respiratory alkalosis. Increased levels of metabolic acids (especially lactic acid) were critical to brain pHi regulation during the initial hour of respiratory alkalosis and accounted for much of the independent effect of hypoxemia on pHi regulation. However, these metabolic acids remained unchanged as pHi was more completely regulated between 1 and 5 h of continued hypocapnia or hypoxic hypocapnia. This time-dependent regulation of pHi may involve some regulatory role for changed transmembrane fluxes of H+ and/or HCO3-. Significant interregional differences were observed in both pHi and in ECS; with tendencies toward more alkaline pHi and lower ECS in brain stem and white matter. With respiratory alkalosis ECS fell and intracellular fluid increased in both cortex and caudate nucleus, possibly reflecting an osmotic effect of increased metabolic acid levels or reduction in cell membrane ion pumping.
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PMID:Interregional differences in brain intracellular pH and water compartmentation during acute normoxic and hypoxic hypocapnia in the anesthetized dog. 678 4