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

The effect of sustained hypercapnia on the acid-base balance and gill ventilation in rainbow trout, Salmo gairdneri, was studied. The response to an increase in PICO2 from 0.3 to 5.2 mm Hg was a five-fold increase in gill ventilation volume and a slight increase in breathing frequency. There was a concomitant rise in PACO2 and an immediate fall in pHa. If PICO2 was maintained at 5.2 mm Hg for several days, ventilation volume gradually returned to the initial, prehypercapnic level within three days. Arterial pH also returned to the initial level within 2-3 days. These results are consistent with the hypothesis that under these conditions fish regulate pH via HCO3/C1 exchange across the gills rather than by changes in ventilation and subsequent adjustment of PACO2. A reduction in environmental pH causes a reduction in pHa but only a slow gradual increase in VG. Injections of HC1 or NaHCO3 into the blood have opposite effects on pHa but both cause a marked increase in VG. It is concluded that a rise in PACO2 results in a rise in VG and that changes in pH in blood or water have little direct effect on VG in rainbow trout. Possible location for receptors involved in this reflex response are discussed.
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PMID:The effects of changes in pH and PCO2 in blood and water on breathing in rainbow trout, Salmo gairdneri. 0 Jul 53

To study the role of carbonic anhydrase in the CSF [HCO3] increase in respiratory acidosis and its effect on brain ammonia, anesthetized rats were subjected to hypercapnia (7% CO2) for 2 hours. The animals received periodic intraventricular injections of either 'mock' CSF or 'mock' CSF and acetazolamide for 45 minutes prior and during hypercapnia when: (a) plasma [HCO3-] was allowed to increase normally and (2) plasma [HCO3] increase was prevented by i.v. HC1 infusion, CSF [HCO3] increased 8.5 mM/L after 2 hours of hypercapnia (delta PCO2 40) in the rats with intraventricular 'mock' CSF injections, and only 6 mM/L in the animals with acetazolamide injections. CSF [HCO3-] increased 7 mM/L during hypercapnia and HCl infusion with intraventricular 'mock' CSF injections, but only 2 mM/L with acetazolamide injections. Changes in total brain CO2 (increase) and brain glutamic acid (decrease) in hypercapnia were not affected by intraventricular acetazolamide and i.v. HCl. The increase of brain NH4+ and glutamine in hypercapnia was reduced in these conditions. It is concluded that there are at least two sources for the CSF [HCO3-] increase in hypercapnia; one formed in the CNS and dependent on carbonic anhydrase, and the other derived from plasma [HCO3-] increase.
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PMID:The CSF HCO3 increase in hypercapnia relationshp to HCO3, glutamate, glutamine and NH3 in brain. 1 66