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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

Glutamic, aspartic, and gamma-aminobutyric acid (GABA), glutamine, and ammonium were measured in the brains of unanesthetized normocapnic and hypercapnic (10% CO2; 5 min to 3 wk) rats. Hypercapnia increased glutamine and GABA and decreased glutamic and aspartic acids. Changes occurred within 1 h and were maintained during the observation period of 3 wk. On return to normocapnia amino acid concentrations were almost normal after 1 h. Based on the time course it is concluded that intracerebral hypercapnia is more likely the stimulus for change than acidosis. Ammonium content was unchanged for at least 1 h after the onset of hypercapnia but increased thereafter. Experiments in which glutamine synthesis by brain was impeded by inhibiting the enzyme glutamine synthetase favor the hypothesis that the rise of ammonium content in hypercapnia is initially not seen because of increased glutamine synthesis. The changes observed may have a role in metabolic pH homeostasis of brain tissue and may also be relevant to the modified brain excitability in hypercapnia.
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PMID:Selected brain amino acids and ammonium during chronic hypercapnia in conscious rats. 63 72

In rats, the phenomenon of considerable increase in resistance to acute hypoxia observed after 2-hour stay under conditions of gradually increasing concentration of CO2, decreasing concentration of O2, ANd external cooling at 2--3 degrees seems to be based mainly on changes in concentration of CO2 (ACCORDINGLY, PCO2 and other forms of CO2 in the blood). The high resistance to acute hypoxia develops as well after subcutaneous or i.v. administration of 1.0 ml of water solution (169.2 mg/200 g) NaHCO2, (NH4)2SO4, MgSO4, MnSO4, and ZnSO4 (in proportion: 35 : 5 : 2 : 0.15 : 0.15, resp.) or after 1-hour effect of increased hypercapnia and hypoxia without cooling.
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PMID:[Role of CO2 fixation in increasing the body's resistance to acute hypoxia]. 72 Jun 76

Hyperammonemia increases brain glutamine levels, causes astrocytic swelling, and depresses cerebral blood flow (CBF) responsivity to CO2. Methionine sulfoximine (MSO) inhibition of glutamine synthetase activity, known to be enriched in astrocytes, prevents ammonia-induced increases in brain glutamine and water content. We tested the hypothesis that inhibition of glutamine accumulation restores CBF responsivity to CO2 during acute hyperammonemia. Pentobarbital-anesthetized rats treated with either vehicle or MSO (150 mg/kg i.p.) received a 6-hour intravenous infusion of either sodium or ammonium acetate. With subsequent induction of hypercapnia, CBF increased from 113 +/- 14 (mean +/- SEM) to 194 +/- 9 ml/min per 100 g in control rats but was unchanged from 107 +/- 13 to 79 +/- 10 ml/min per 100 g in hyperammonemic rats. Treatment with MSO in hyperammonemic rats restored the CBF response to hypercapnia (from 73 +/- 8 to 141 +/- 14 ml/min per 100 g). With induction of hypocapnia, CBF decreased from 114 +/- 11 to 88 +/- 11 ml/min per 100 g in control rats but increased from 112 +/- 13 to 142 +/- 19 ml/min per 100 g in hyperammonemic rats. Treatment with MSO in hyperammonemic rats did not fully restore the response to hypocapnia but prevented the paradoxical increase in CBF (from 80 +/- 8 to 80 +/- 8 ml/min per 100 g). In control rats, MSO did not affect CO2 responsivity. Treatment with MSO prevented ammonia-induced increases in intracranial pressure. Hyposmotic-induced increases in brain water content and intracranial pressure attenuated the CBF response to hypercapnia but, unlike hyperammonemia, did not attenuate the response to hypocapnia. In contrast to hypercapnia, vasodilation in response to arterial hypotension was intact in hyperammonemic rats. We conclude that the grossly abnormal CBF responsivity to CO2 alterations during hyperammonemia is linked to glutamine accumulation rather than ammonia per se. Cerebral edema secondary to glutamine accumulation may contribute in part to abnormal CBF responses, although other aspects of astrocyte dysfunction are likely to be important.
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PMID:Restoration of cerebrovascular CO2 responsivity by glutamine synthesis inhibition in hyperammonemic rats. 139 82

We measured intracellular pH (pHi) of single epithelial cells in situ in the urinary bladder epithelium using microspectrofluorometry and the cytoplasmically trapped pH-sensitive fluorophore, 2',7'-bis(2-carboxyethyl)-5(6)- carboxyfluorescein (BCECF). The resting pHi was 7.21 +/- 0.03 (n = 40 bladders, 489 cells) in pH 7.8 bathing solutions, indicating that H+ is not passively distributed across the plasma membrane and is extruded against its electrochemical gradient. Whereas exposure to hypercapnia (5% CO2 saturation) reversibly decreased pHi, mucosally added 20 mM NH4+ reversibly increased pHi. Recovery from the NH4+ effect was slow and lacked an acid-load pHi undershoot; this is interpreted as suggesting significant NH4+ permeability. Recovery from hypercapnic acidosis was blocked by mucosally added amiloride, indicating that apical Na(+)-H+ exchange is involved in pHi regulation. Addition of 0.5 mM NH4+ to the basolateral side when the mucosal side was bathed in mock urine (2 mM NaCl) significantly increased undirectional mucosal-to-serosal Na+ flux, and the increase was blocked by mucosally added amiloride. We conclude that an apically located Na(+)-H+ exchange is important in pHi regulation and may also accept NH4+ as the counterion for Na+.
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PMID:Intracellular pH regulation in trout urinary bladder epithelium: Na(+)-H+(NH4+) exchange. 165 43

The purpose of this study was to determine how changes in ventilation rate and in the entry route of air pollutants into the respiratory tract (nose versus mouth breathing) affected the respiratory tract uptake and penetration of inhaled gaseous and particulate pollutants associated with automobile emissions. Experiments were performed with female beagle dogs exposed while standing at rest or while exercising on a treadmill at 5 km/hour and a 7.5 percent grade. Dogs were exposed to nitrogen dioxide at concentrations of 1 and 5 parts per million (ppm), to formaldehyde at 2 and 10 ppm, and to an aerosol of ammonium nitrate particles (0.3 micron mass median aerodynamic diameter) at 1 mg/m3. Total respiratory system uptake and effects on breath time, expired tidal volume, fractional expiration time, minute ventilation, respiratory gas exchange, ventilation equivalents for oxygen and carbon dioxide, and dynamic pulmonary resistance and compliance were measured in exercising and resting dogs exposed for two hours to 5 ppm nitrogen dioxide and 10 ppm formaldehyde in combination with 1 mg/m3 of ammonium nitrate particles. Regional penetration of pollutants through oral and nasal airways and pollutant uptake in the lung were measured in a separate group of six tracheostomized dogs standing at rest while being exposed to nitrogen dioxide, formaldehyde, and ammonium nitrate particles. Hypercapnic stimulation was used to modify ventilation rates in the tracheostomized dogs while pollutant penetration and uptake were measured. Dogs exposed to 5 ppm of nitrogen dioxide at rest tended to breathe more rapidly (p less than 0.05) and more shallowly (a nonsignificant trend) than dogs exposed to purified air. The changes observed were similar in direction, but of smaller magnitude, to changes observed when the same dogs were exposed during exercise to ozone at 0.6 ppm in a separate study. Rapid-shallow breathing was not observed when the dogs were exposed during exercise to 5 ppm nitrogen dioxide. Dogs exposed to a mixture of 10 ppm formaldehyde and 1 mg/m3 ammonium nitrate particles during exercise showed a shift to larger tidal volume breathing, but the response was much less pronounced than the slow-deep breathing pattern response observed in a separate study of dogs exposed to 10 ppm formaldehyde alone. The total respiratory system uptake of formaldehyde from the formaldehyde and ammonium nitrate mixture was larger than that measured for 10 ppm of formaldehyde alone in another exercise and exposure study.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The effects of exercise on dose and dose distribution of inhaled automotive pollutants. 172 1

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

Several disturbances of acid-base balance, including chronic metabolic and respiratory acidoses and metabolic alkalosis, are associated with enhanced proximal tubule bicarbonate reabsorption. To determine whether augmented brush border Na/H exchange might mediate enhanced proximal tubule bicarbonate reabsorption in these disorders, we measured Na/H exchange activity in cortical brush border membrane vesicles (BBMV) prepared from rats and rabbits adapted to hypercapnia and other chronic acid-base disturbances. BBMV prepared from control animals and animals with chronic acid-base disturbances were similar as judged by marker enzymes, alkaline phosphatase, and ouabain-sensitive phosphatase. Despite profound respiratory acidosis, no increase in Na/H exchange activity could be detected in vesicles prepared from rats adapted to chronic (8 to 10 days) or subacute (24 hr) respiratory acidosis. In addition, vesicles prepared from rabbits exposed to chronic hypercapnia did not show increased Na/H exchange when compared with contemporaneous controls. By contrast, in agreement with previously published results, amiloride-sensitive sodium uptake was increased by 30% in vesicles derived from animals with ammonium chloride-induced acidosis compared with contemporaneous controls. Two models of chronic metabolic alkalosis were also studied; vesicles from alkalotic rats did not show any alteration in Na/H exchange. We conclude that metabolic acidosis, but not respiratory acidosis or metabolic alkalosis, leads to enhanced activity of the luminal Na/H exchanger.
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PMID:Regulation of Na/H exchange in renal microvillus vesicles in chronic hypercapnia. 284 83

To study both temporal and quantitative effects of hypercapnia on the extent of pH compensation in the arterial blood, specimens of carp (Cyprinus carpio) were exposed to a PCO2 of about 7.5 mmHg (1 mmHg = 133.3 Pa) (1% CO2) in the environmental water for several weeks, and a second group of animals was subjected to an environmental PCO2 of about 37 mmHg (5% CO2) for up to 96 h. A third series of experiments was designed to test the possibility that infusion of bicarbonate would increase the extent of plasma pH compensation. Dorsal aortic plasma pH, PCO2 and [HCO3-], as well as net transfer of HCO3- -equivalent ions, NH4+, Cl- and Na+, between fish and ambient water, were monitored throughout the experiments. Exposure to environmental PCO2 of 7.5 mmHg resulted in the expected respiratory acidosis with the associated drop in plasma pH, and subsequent compensatory plasma [HCO3-] increase. The compensatory increase of plasma bicarbonate during long-term hypercapnia continued during 19 days of exposure with plasma bicarbonate finally elevated from 13.0 mmoll-1 during control conditions to 25.9 mmoll-1 in hypercapnia, an increase equivalent to 80% plasma pH compensation. Exposure to 5% hypercapnia elicited much larger acid-base effects, which were compensated to a much lesser extent. Plasma pH recovered to only about 45% of the pH depression expected at constant bicarbonate concentration. At the end of the 96-h exposure period, plasma [HCO3-] was elevated by a factor of 2.5 to about 28.2 mmoll-1. The observed increase in plasma bicarbonate concentration during 5% hypercapnic exposure was attributable to net gain of bicarbonate equivalent ions from (or release of H+-equivalent ions to) the environmental water. Quantitatively, the gain of 15.6 mmol kg-1 was considerably larger than the amount required for compensation of the extracellular space, suggesting that acid-base relevant ions were transferred for compensation of the intracellular body compartments. The uptake of bicarbonate-equivalent ions from the water was accompanied by a net release of Cl-and, to a smaller extent, by a net uptake of Na+, suggesting a 75% contribution of the Cl-/HCO-3 exchange mechanism. Infusion of bicarbonate after 48 h of exposure to 7.5 mmHg PCo2 had only a transient effect on further pH compensation. The infused bicarbonate was lost to the ambient water, and pre-infusion levels of bicarbonate were reattained within 24 h. Repetition of the infusion did not result in a notable improvement of the acid-base status.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acid-base regulation and ion transfers in the carp (Cyprinus carpio): pH compensation during graded long- and short-term environmental hypercapnia, and the effect of bicarbonate infusion. 302 33

We previously showed that rats made hypoxic for three weeks were able to regulate their plasma pH better than normoxic rats during acute hypercapnia. This improved pH regulation was abolished by nephrectomy, suggesting that it was due, at least in part, to a more effective renal compensation of hypercapnia in hypoxic rats. To test this possibility renal acid excretion was measured in conscious rats that had been kept at PB 370-380 Torr for three weeks. The rats were studied in a chamber where PIO2 was kept at 68-70 Torr at ambient PB (740-750 Torr). Controls were pair-fed normoxic rats. After a 2 h control period, inspired PCO2 was increased for 4 h. The apparent non-bicarbonate buffer value of arterial blood plasma was twice as high in the hypoxic than in the normoxic rats. Renal excretion of ammonium increased to a similar extent during hypercapnia in both normoxic and hypoxic rats. Titratable acid excretion of normoxic rats did not change significantly during hypercapnia. In the hypoxic rats, on the other hand, total excretion of titratable acid in the 2 h control period was 90.9 +/- 16.4 mumol/rat; and increased to 150.0 +/- 13.4 mumol/rat in the first 2 h and to 232.9 +/- 26.0 mumol/rat in the last 2 h of hypercapnia. In spite of this large increase in acid excretion, urine pH of hypoxic rats did not change significantly, indicating a higher buffer value of the urine of hypoxic rats. These results confirm our previous observations and support the idea that the improved pH regulation of hypoxic rats is due in part to a more effective renal compensation of hypercapnia.
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PMID:Renal compensation of hypercapnia in prolonged hypoxia. 309 73


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