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

In the present study we investigated if an amiloride inhibitable Na+ -H+ exchange mechanism may also be involved in the regulation of cisternal cerebrospinal fluid (CSF) [HCO3-] during acute respiratory acidosis (ARA). In anesthetized, paralyzed and ventilated dogs either mock CSF (group I, control) or mock CSF containing amiloride (group II) was injected into the cerebral lateral ventricles and ARA was induced by 8-10% CO2 breathing during 4 1/2 hours. During hypercapnia arterial PCO2 and plasma [HCO3-] rose respectively by about 35 mm Hg and 3 mmol/L in both groups. The rise in cisternal CSF PCO2 (about 40 mm Hg) was similar. However, changes in CSF [HCO3-] were significantly different between the two groups; in the control group, mean CSF [HCO3-] rose by 2.4, 4.1 and 4.4 mmol/L respectively, 1 1/2, 3 and 4 1/2 h after induction of ARA. In the amiloride group the respective rise was only 1.1, 2.5 and 2.5 mmol/L. The differences in CSF [HCO3-] could not be ascribed to differences in CSF lactate concentration. We conclude that an amiloride inhibitable Na+ -H+ exchange may play a role in the regulation of CSF [HCO3-] during acute respiratory acidosis in dogs.
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PMID:Effect of amiloride on cisternal fluid [HCO3-] in acute respiratory acidosis. 644 Feb 51

Intracellular pH (pHi) of triceps, trapezius, quadriceps and gastrocnemius muscle tissue was determined in rats with myocardial hypertrophy due to experimental aortic stenosis (AS) and in sham operated rats (SO). During normocapnia, no significant difference in pHi between AS and So animals was observed in any of the muscle species investigated. In hypercapnia (FICO2 0.06, 0.075 or 0.100) pHi of AS was significantly higher than pHi of SO in all muscles, despite no difference in pHe, PaCO2 or [HCO3]a between AS and SO. Therefore, AS appears to be associated with an improvement of pHi regulation in skeletal muscle. In this respect, skeletal muscle behaves as hypertrophic cardiac muscle, which also shows an increased ability to regulate pHi in AS. These results suggest that the changes in pHi regulation of hypertrophic myocardium are not due to the hypertrophic process per se, but to a general phenomenon secondary to AS.
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PMID:Changes in intracellular pH regulation of skeletal muscle of rats with aortic stenosis. 646 Mar 6

Ventilation and cisternal cerebrospinal fluid (CSF) and arterial acid-base balance were measured in awake dogs during air control and from 1 h to 26 days of breathing 5% CO2 in air. Ventilation increased 4-fold during acute hypercapnia and then declined to a minimum at 5-10 days. Between 1-3 days and 16-26 days of hypercapnia ventilation was relatively stable at 2.5 times control. [HCO3-]CSF increased rapidly by 12 h of hypercapnia and in the steady-state [HCO3-]CSF was correlated with PCSFCO2. Between 1 h and 1.5 days of hypercapnia, increase in [HCO3-]CSF was also correlated with increase in [NH3]CSF. Despite increase in [HCO3-]CSF, there was no compensation of [H+]CSF throughout 26 days of hypercapnia. Hydrogen ion may have contributed to the control of ventilation during chronic hypercapnia since ventilation was correlated with [HCO3-]a and [HCO3-]CSF. However, a relationship between ventilation and [H+] of arterial blood and CSF during chronic hypercapnia was relatively poor or absent. Ventilatory adaptation to chronic hypercapnia could not be related to metabolism or to [NH3]CSF. The mechanism(s) by which the increase in PCO2 during chronic respiratory acidosis results in sustained elevation of ventilation remains to be resolved.
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PMID:Acid-base and ventilatory adaptation in conscious dogs during chronic hypercapnia. 652 12

Specimens of Conger conger (L.) were exposed to environmental hypercapnia in a closed recirculating seawater system. Arterial plasma pH, PCO2 and bicarbonate concentration, as well as the net transfer of bicarbonate and ammonia between fish and ambient seawater, were monitored for 30 h of hypercapnia. The initial hypercapnia-induced reduction of arterial pH by about 0.4 pH units was restored to near control values within 10 h of hypercapnia by compensatory elevation of plasma bicarbonate concentration. The continuous rise in extracellular bicarbonate from about 5 to 22 mM during this time was the result of two different mechanisms. Initially, there was a net bicarbonate transfer from the intracellular space to the extracellular compartment until the net uptake of bicarbonate from the seawater started. The amount of bicarbonate originally transferred to the extracellular space was then returned to the intracellular compartment and finally the changes in both extracellular and intracellular pH were compensated by bicarbonate taken up from the environmental seawater. Since the ammonia excretion was not increased during hypercapnia and the pattern of plasma electrolyte concentrations does not favour the H+/Na+ ion exchange mechanism, it is concluded that the additional bicarbonate is gained by active HCO3-/Cl- ion exchange against the electrochemical gradient between fish and seawater.
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PMID:Regulation of the acid-base status during environmental hypercapnia in the marine teleost fish Conger conger. 666 65

In the unanesthetized dogfish, Scyliorhinus canicula, oxygen and carbon dioxide partial pressures and concentrations in inspired and expired water and the acid-base balance of arterial blood, pHa and PcCO2, were determined. Each dogfish was exposed to waters differing in oxygenation and in CO2 levels, which was controlled with a pH-CO2-stat device, for successive 2- to 3-h periods. The four ambient conditions were: normoxia-normocapnia (inspired PO2, PIO2 ca 160 Torr; PICO2 ca 0.3 Torr), hyperoxia-normocapnia (PIO2 ca 730 Torr), hyperoxia-hypercapnia (PICO2 ca 1.0 Torr); normoxia-hypercapnia. At both low and high ambient CO2, the inspired-expired O2 and CO2 concentration differences increased in hyperoxia. Ventilation was depressed, and concomitantly, PACO2 increased and the arterial plasma pH decreased. The hypercapnic acidosis was rapidly but only partially compensated by an increase of the plasma bicarbonate concentration. Due to the buffer action of carbonate in sea water, low and high ambient CO2 levels corresponded respectively to high and low values of the CO2 capacitance coefficient, betaWCO2. At both ambient oxygenation levels, the expired-inspired PCO2 difference was greater at low than at high betaWCO2. At a given ambient CO2 level, expired PCO2, PECO2, wash higher in hyperoxia than in normoxia; an effect more marked at low than at high betaWCO2. Thus, the water capacitance coeffcient betaWCO2 is an important factor determining PECO2 values and probably arterial blood acid-base balance. As a general conclusion, the acid-base balance of the arterial blood in the dogfish is very much dependent on the conditions of the oxygenation and acid-base balance of the ambient water which consequently should be carefully controlled.
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PMID:Blood acid-base balance as a function of water oxygenation: a study at two different ambient CO2 levels in the dogfish, Scyliorhinus canicula. 677 56

Rats were exposed to 11% CO2 in air for 15 min or 3 h and measurements made of ventilation, CSF acid-base values, and blood, CSF and brain electrolytes. Brain tissue HCO3- was studied by performing CO2 titration curves of tissue homogenates in vitro, the upward displacement of these curves reflecting the non-physico-chemical buffer mechanisms prominent in sustained hypercapnia. At 15 min, the CO2 induced increase in [HCO3-] was accompanied in CSF by an equimolar increase in [Na+] and in brain tissue by an increase in [K+]. At 3 h, the further increase in [HCO3-] was accompanied in CSF by a smaller increase in [Na+] and a decrease in [Cl-] and in brain tissue, there were no longer any significant changes in monovalent ions. In brain, the immediate pH regulatory response to hypercapnia appears to involve physico-chemical buffering and an ionic exchange with blood while by 3 h, the further increase in cell HCO3- must reflect altered cell metabolism. In CSF, the immediate increase in [Na+] and [HCO3-] is probably via choroid plexus while by 3 h, the CSF [HCO3-] increase could reflect exchange with blood at non-choroidal sites or to a less likely extent exchange with brain cells. CSF and brain cell pH regulation is reflected in ventilation which is lower at 3 h than at 15 min of CO2 exposure.
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PMID:Brain and cerebrospinal fluid ionic composition and ventilation in acute hypercapnia. 677 43

On day 16 of the chick embryo, a catheter was implanted in the allantoic vein carrying arterialized blood, and a syringe was attached to the blunt end of the shell connecting to the air cell. This technique allowed for repetitive sampling and analysis of air cell gas and arterialized blood when these eggs were exposed to a He-O2 or SF6-O2 atmosphere. Exposure to He-O2 reduced the arterial CO2 tension(PaCO2) from 36 to 17 Torr and increased pH by 0.17 units; exposure to SF6-O2 increased PaCO2 from 37 to 62 Torr and reduced the pH by 0.14 units. These responses were brought about by changes in the gas conductance of the shell, resulting in a diffusive hypocapnia and respiratory alkalosis in He-O2 and a diffusive hypercapnia and respiratory acidosis in SF6-O2. During a 4-h exposure to these foreign gases the observed pH changes were smaller than predicted because of marked shifts of HCO3- into the blood (SF6-O2) or out of the blood (He-O2).
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PMID:Changes in acid-base balance of chick embryos exposed to a He or SF6 atmosphere. 679 Apr 88

When blood in the pulmonary capillary is oxygenated in hypercapnic air, PCO2 in the red cell has been thought to exceed alveolar PCO2 due to the Haldane effect, inducing outward CO2 diffusion. As long as the inward CO2 diffusion and, consequently, HCO3- formation are prevented in the red cell, the CO2 gain in plasma is reduced down to the level predicted from a CO2 dissociation curve of separated plasma. Therefore, if the direction of the CO2 diffusion is not reversed during the contact time, the virtual venous PCO2 (PEq), where the CO2 loss due to the Haldane effect is balanced with the gain due to the venoalveolar PCO2 gradient, becomes higher than the oxygenated venous PCO2 in proportion to the CO2 difference between the true and separated plasma. In order to verify the validity of the above assumption, the PEq value was measured in normo- and hypercapnia by using the Defares' extrapolation method in six normal subjects. The results obtained revealed that the PEq estimated in hypercapnia was obviously higher than that in normocapnia. The above difference was significantly greater in normoxia than in hypoxia. Furthermore, it agreed fairly well with the theoretical difference presumed by taking the difference in CO2 content between separated and true plasma and the R. Q. effect on the alveolar gas volume into account, suggesting that the inward CO2 diffusion following the oxygenation reaction could be disregarded in normoxic hypercapnia.
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PMID:The influence of the Haldane effect on alveolar CO2 tension equilibrated with mixed venous blood in man. 679 74

When mixed venous blood is oxygenated in alveolar air with higher PCO2, the PCO2 within the red cell is though to exceed the alveolar PCO2 due to the Haldane effect and to block the inward CO2 diffusion. If the direction of the CO2 diffusion is not reversed during the contact time, the HCO2-gain in the plasma will not exceed the amount estimated from venoalveolar PCO2 difference by using a CO2 dissociation curve of separated plasma. In order to clarify the validity of the above thought, the venoarterial CO2 content difference was measured by using a van Slyke apparatus and a PCO2 electrode at various alveolar PCO2 levels in rebreathing dogs. The HCO3-rise in the whole blood was obviously reduced when acute hypercapnia was administered in both normoxia and hyperoxia. Quantitatively, the decrease of CO2 content under hypercapnia corresponded to the difference in CO2 content between the true and separated plasma. The reduction, however, was slightly stronger in normoxia than in hyperoxia with alveolar PO2 of 300 to 420 mmHg. These data seem to support the following explanation: When venous blood was oxygenated in normoxic air with PCO2 higher than true venous, the inward CO2 diffusion was inhibited by the Haldane effect and the reversed diffusion after the oxygenation could also be disregarded during the contact time. Because the oxygenation was accelerated in hyperoxia and the direction of the CO2 diffusion was reversed earlier than in normoxia, the plasma CO2 content became higher in hyperoxia than in normoxia.
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PMID:Relationship between venoarterial CO2 content difference and venoalveolar PCO2 difference in acute hypercapnia in dogs. 679 75

(1) The scope of this review is to examine the experimental evidence for the existence of negative PCO2 differences between pulmonary capillary blood and lung gas, [delta PCO2(b-G)], which have been observed both during rebreathing, when CO2 was at equilibrium, and during steady state gas exchange, particularly in hypercapnia. (2) The mechanism that have been invoked to explain negative delta PCO2(b-G) include (i) slow equilibration of the system CO2/HCO3-/H+ in blood, and (ii) effects of a negatvely charged surface of the pulmonary capillary endothelium. While the first postulated mechanism appears to be quantitatively insufficient to explain the results, the second seems to lead to serious qualitative difficulties. (3) Existence of negative delta PCO2(b-G) in CO2 equilibrium would invalidate the basis of the conventional analysis of alveolar gas exchange. (4) A critical analysis of the experimental evidence for the existence of negative delta PCO2(b-G) is presented. It includes the identification of directional experimental errors leading to spurious negative delta PCO2(b-G), and a critical review of the literature data in this regard. (5) Results of own experiments, conducted in an attempt to consider all possible sources of error, are reported, revealing (i) perfect PCO2 equality between alveolar gas and blood in rebreathing equilibrium of CO2; (ii) absence of negative delta PCO2 (b-G) during steady state gas exchange in hypercapnia. (6)Both experiments and model calculations show that negative delta PCO2 between mixed venous blood and end-expired gas observed in birds at steady state of gas exchange are explained by a particular action of the Haldane effect in avian parabronchial lungs with cross-current arrangement of gas and blood flow. (7) It is concluded that the negative delta PCO2(b-G) reported in the literature are probably artifactual and that there is no adequate evidence to invalidate the traditional view according to which blood/gas CO2 equilibration in lungs leads to equal PCO2 in both media.
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PMID:Blood/gas equilibrium of carbon dioxide in lungs. A critical review. 698 19


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