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

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

The carotid bodies appear to be the only peripheral chemoreceptors mediating ventilatory control during exercise in man. While little is known about the mechanism of stimulation, much is known about the effects of carotid body stimulation upon pulmonary ventilation (VE). These effects have been produced by hypercapnia, hypoxia, metabolic acidosis, arterial blood pressure, temperature, and catecholamines. A signal from CO2 flow is attractive because of the strong correlation between CO2 output and VE during exercise. The carotid body's role in the hyperpnea depends on the intensity of exercise. During heavy exercise, pH falls and hyperventilation ensues. The carotid bodies appear to be the exclusive mediators of the ventilatory compensation for the acidosis at this exercise intensity. For moderate exercise, mean arterial PCO2 does not change. Therefore, how is the CO2 signal transmitted to the respiratory center? Two current theories are: (1) since arterial PCO2 and pH oscillate with each breath, the amplitude and period of these oscillations may change during exercise and may be of sufficient magnitude to stimulate the carotid bodies, and (2) there exists a disequilibrium between hydrogen ion activity within the red blood cell and in the plasma because carbonic anhydrase is found in the former but not the latter. This theory assumes that the enzyme is not accessible to the plasma.
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PMID:Peripheral chemoreceptors and exercise hyperpnea. 4 92

The experiments on 18 guinea pigs were divided into two groups and each group was arranged in such a way that the effect of hypercapnia (generated by breathing 10% CO2-90% O2) was investigated with and without inhibition of carbonic anhydrase by methazolamide, 25 mg/kg, in the first group and acetazolamide, 50 mg/kg, in the second group, administered intravenously. The endocochlear potentials (EP) and endocochlear PO2 were recorded by microelectrodes introduced into the scala media, and cochlear microphonics (CM) were monitored by a silver-wire electrode from the round window. In the first exposure to hypercapnia (20-40 min) EP increased about + 6 mV. At the same time CM decreased; the reason for this is not yet known. During the second period of hypercapnia (80-100 min) when carbonic anhydrase was inhibited with methazolamide and acetazolamide, EP did not elevate as during the first period when carbonic anhydrase was not inhibited. In this work, under specific conditions, it was observed for the first time that carbonic anhydrase affects the generation of EP.
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PMID:Carbonic anhydrase in the generation of cochlear potentials. 10 17

A specific and quantitative immunological method for the determination of human erythrocyte carbonic anhydrase (HCA) isoenzyme B has been used to determine the contents of enzyme in the erythrocytes from healthy persons and from subjects with chronic obstructive lung disease. The investigations have shown a statistically significant increase of HCA type B in the erythrocytes of subjects suffering from chronic obstructive lung disease and hypercapnia. Subjects with chronic obstructive lung disease and normal PaCO2 showed no difference from normal subjects. No correlation was found between PaCO2 and human erythrocyte carbonic anhydrase.
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PMID:Carbonic anhydrase isoenzyme B in erythrocytes of subjects with chronic obstructive lung disease. 10 3

It is accepted that in hypercapnia the rise in cerebrospinal fluid bicarbonate concentration (CSF [HCO3-]) occurs because of local HCO3--generating mechanisms, dependent on carbonic anhydrase, as well as on diffusion of HCO3- from plasma. To investigate further the regulation of CSF [HCO3-], CSF HCO3- formation was studied under conditions of pure isocapnic CSF "metabolic" acidosis. In anesthetized normocapnic dogs CSF [HCO3-] was lowered to approximately 15 mmol/l by perfusing the brain ventricles with a low HCO3- solution for 45 min. In dogs with normal plasma [HCO3-], CSF [HCO3-] rose by approximately 7 mmol/l in 2 h after the end of the perfusion. Lowering plasma [HCO3-] to 10 mmol/l by infusing HCl, limited the CSF [HCO3-] rise to 2 mmol/l, indicating the importance of plasma HCO3- for the restoration of CSF [HCO3-]. The small and persistent rise of CSF [HCO3-] at low plasma [HCO3-] occurred against a concentration gradient with blood. Intraventricular injection of acetazolamide had no further effect on this small rise. It is concluded that under the conditions of our experiments the CSF [HCO3-] rise is significantly dependent on plasma [HCO3-] and the caronic anhydrase-dependent HCO3- generation in the CNS is less important.
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PMID:Restoration of CSF [HCO3-] after its experimental lowering in normocapnic conditions. 11 88

The effects of elevated plasma CO2 partial pressure (PCO2) and [HCO3-] on cerebrospinal fluid (CSF) HCO3- accession have been reviewed in the context of the basal route of CSF HCO3- formation. The basal rate of 53 mM/h appears to be a consequence entirely of formation, via the reaction CO2 + OH- leads to HCO3-. Two-thirds of this rate is catalyzed by carbonic anhydrase, and the remainder uncatalyzed. The HCO3- accession matches 37% that of sodium, so that the HCO3- rate is involved with CSF turnover. When PCO2 is elevated twofold, the rate of HCO3- formation increase 10%, and results in elevation of CSF [HCO3-] by 5 mM in 1 h. Also, when plasma [HCO3-] is elevated 15 mM, CSF [HCO3-] rises about 5 mM/h; this is transfer of HCO3- "as such" by diffusion from plasma. The effects of hypercapnia and metabolic alkalosis on CSF HCO3- accumulation are additive, but they occur by separate processes. The effect of hypercapnia is an exaltation of the normal process due to increased substrate (CO2), but that of increased plasma HCO3- is due to imposition of an abnormal diffusion gradient for this ion between plasma and CSF. The effect of hypercapnia in elevating brain HCO3- operates to maintain brain pH and is also based on the formation of HCO3- from CO2. Brain HCO3- may also be a source of CSF HCO3-. Relations have been sought between the chemically calculated rates of HCO3- formation in CSF and those observed. The chemically calculated catalytic rate is 1,600 times greater than that observed, agreeing with the fact that more than 99.9% of choroid plexus carbonic anhydrase must be inhibited to yield a decrease in fluid formation or ion transport from plasma to CSF. The calculated uncatalyzed rate agrees closely with what is observed after complete inhibition of the enzyme. These considerations support the idea that all the HCO3- reaching the CSF is formed from CO2, rather than by transfer of the ion from plasma to CSF.
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PMID:Effect of varying CO2 equilibria on rates of HCO3- formation in cerebrospinal fluid. 11 42

Using the stop flow microperfusion technique with simultaneous capillary perfusion the secretory rate of H+ ions in the proximal tubule was evaluated by measuring the level flow reabsorption as well as the static head concentration difference of 3H labeled glycodiazine. At ambient glycodiazine concentration of 21 mmol/l the level flow reabsorption is in the same range as that of bicarbonate. In the early proximal loops the reabsorption is 20% greater than in the late proximal loops. The carbonic anhydrase inhibitors acetazolamide and 3,4-methylene-dioxyphenyl-sulfonamide (both 10(-4) M) as well as furosemide (10 (-3) M) inhibit the glycodiazine reabsorption 43%, 27% and 22% respectively. Thiocyanate (2-10(-2) M), however, exerted only an insignificant inhibition (12%). When Na+ in the ambient perfusion solutions was replaced by Li+ or choline+ the glycodiazine transport was strongly reduced. Ouabain (5-10(-2) M) inhibited too, but amiloride (10(-3) M) had no effect on glycodiazine transport. The glycodiazine transport was 28% reduced in metabolic alkalosis and to a smaller although significant extent (17%) in metabolic acidosis; it was unchanged in chronic hypercapnia. In chronic K+ depletion the glycodiazine reabsorption was accelerated by 12% only in the early proximal loops. Chronic parathyroidectomy as well as acute substitution with parathyroid hormone had no effect on the glycodiazine absorption. The main conclusions are: Proximal H+ transport proceeds with suitable buffers. Although independent of HCO3- and carbonic anhydrase, it could be partially inhibited by CA inhibitors. H+ transport is supposed to proceed as countertransport with Na+ ions. In chronic alkalosis the H+ transport is reduced.
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PMID:Renal proximal tubular buffer-(glycodiazine) transport. Inhomogeneity of local transport rate, dependence on sodium, effect of inhibitors and chronic adaptation. 12 86

After a three day-period of hypercapnia, carbonic anhydrase blockade by acetazolamide inhibits the development of arterial blood alcalosis during the return in normal environment, and thus eliminates the transient increase in lactacidemia due to glycolysis stimulation.
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PMID:[Effect of acetazolamide on arterial blood lactate levels during recuperation in air from three days of hypercapnia]. 24 68

The activity and the isozyme B and C levels of red cell carbonic anhydrase was examined before and during CO2 inhalation in 18 patients with chronic respiratory failure. Carbonic anhydrase B and C levels did not change during 5 min breathing of high (8-9%) and low (3-5%) CO2 mixture. Carbonic anhydrase activity decreased in patients with combined hypercarbia (Paco2 greater than or equal to 45 mmHg) and hypoxemia (Pao2 less than or equal to 60 mmHg). This was accompanied by an increase in red cell K+ content, 2, 3-DPG and Hct/Hb. The activity did not change in patients with only hypoxemia. Carbonic anhydrase activity and plasma HCO-3 concentration were positively correlated (r = 0.4, P less than 0.05). A significant inverse correlation was also found between changes in red cell K+ content and those in carbonic anhydrase activity (r = - 0.42, P less than 0.05). These results indicate that 1), there is a dissociation between activity and isozyme levels in red cell carbonic anhydrase during the initial 5 min of CO2 breathing in patients with combined hypercarbia and hypoxemia, and 2), there seems a linkage exists between K+ movement across the red cell membrane and carbonic anhydrase activity.
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PMID:Effect of CO2 on carbonic anhydrase activity and isozyme levels in respiratory failure. 41 57

The effect of carbon dioxide on oxygen dioxide tension in the endolymph was determined by the micropolarographic technique. Different concentrations (5% and 10% CO2) and different exposure times (3, 5, and 20 minutes) were investigated. The highest levels of PO2 in the endolymph (101.7, 93.9 and 69.5 mm Hg) were accomplished by respiration of 10% CO2, 90% O2, for 20, 5 and 3 minutes consecutively. The lowest PO2 increase, 50.7 mm Hg was observed after breathing 5% CO2, 90% O2 for 20 minutes. Extreme hypercapnia caused an increase of endocochlear potentials (EP) in all groups. In the second group EP increased from +79.3 to +84.9 and in all groups they had returned to the pretreatment level after CO2 discontinuation. These results support the theory that carbonic anhydrase participates in the generation of EP. At the same time that EP increased, cochlear microphonics declined and opposite after the breathing mixture was discontinued. The results permit the conclusion that high levels of PO2 in endolymph is achievable even with short periods of respiration with high CO2 mixture, and suggest the role of carbonic anhydrase during EP generation.
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PMID:Variation of endocochlear PO2 and cochlear potentials by breathing carbon dioxide. 44 16


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