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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

Isolated rabbit hearts were perfused with rabbit red cells suspended in Ringer solution. A small volume of perfusate was recirculated for 10 min at Pco2 of 33.4 +/- 0.9 or 150.8 +/- 7.5 mmHg. Hypercapnia resulted in an increase in perfusate HCO3- concentration that was smaller than that observed when isolated perfusate was equilibrated in vitro with the same CO2 tensions (delta HCO-3e = 1.6 mM, P less than 0.01). This difference is consistent with a net movement of HCO3- into or H+ out of the mycardial cell, and cannot be accounted for by dilution of HCO3- in the myocardial interstitium. Recirculation of perfusate through the coronary circulation at normal Pco2 for two consecutive 10-min periods was not followed by changes in perfusate HCO3- concentration. A high degree of correlation (r = 0.81) was observed between intracellular HCO-3e concentration and the corresponding delta HCO-3e in individual experiments. The results suggest that transmembrane exchange of H+ or HCO3- is a buffer mechanism for CO2 in the myocardial cell.
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PMID:Myocardial CO2 buffering: role of transmembrane transport of H+ or HCO3-ions. 0 80

In order to test the effects of hypercapnia on the acid-base status of fish, larger spotted dogfish were exposed to sudden changes of PCO2 in a closed seawater recirculation system. pH, PCO2 and PO2 were determined in arterial blood and seawater. The exchange of bicarbonate between extracellular space (ECS), intracellular space (ICS), and seawater (SW) was obtained from changes of the total bicarbonate amount in ECS and SW. After fourfold increase of PCO2 arterial pH fell markedly, but started to recover immediately towards control values. This was caused by compensatory accumulation of bicarbonate in the ECS. According to the origin of the extracellular bicarbonate increase three periods could be distinguished: 1.-- Bicarbonate transferred from ICS to both ECS and SW; 2. -- Bicarbonate transferred from both SW and ICS to ECS; 3. -- Bicarbonate transferred from SW to both ECS and ICS. After return to normocapnia similar periods occurred with opposite transfer directions and delayed period transitions. In the first period the ICS was found to be the only source for compensatory bicarbonate increases and even in the second period the ICS contributed to compensation of the extracellular pH. Thus bicarbonate exchange with the ICS appears to be an important regulatory mechanism diminishing the extracellular pH variations after changes in PCO2, before other compensatory mechanisms are initiated.
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PMID:Hypercapnia and resultant bicarbonate transfer processes in an elasmobranch fish (Scyliorhinus stellaris). 1 88

An isolated perfused lung (IPL) preparation was used to investigate the influence of acute environmental stress on lung substrate metabolism. The IPL apparatus consists of four perfusion flasks housed in a temperature-controlled Lucite box with a circulation fan. Lungs are ventilated by a positive pressure ventilation pump. The ventilation is arranged so that the lung can be ventilated with any desired gas composition with concomitant collection of expired gases. The perfusion medium is circulated at 10 ml/min with a peristaltic blood pump, and passes through a specially designed chamber to dampen pulmonary pressure and remove emboli. The perfusion medium presently used in our experiments consisted of washed bovine red blood cells resuspended to a 15% hematocrit with Krebs-Henseleit bicarbonate buffer containing 6% dialyzed Pentex bovine serum albumin. Circulating substrates include 6muM glucose and 0.4muM palmitate. The pH is adjusted to 7.4 with 0.8M Na carbonate. Lungs perfused for 1.5 hr with this apparatus maintain viability, show little edema, maintain blood gases, and show linear incorporation of labeled glucose into lung lipids. Perfused lungs made hypocapnic show a significant (p less than 0.05) rise in lactate and pyruvate, while perfused lungs made hypercapnia show a significant decrease in pyruvate with no change in lactate.
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PMID:Perfused lung preparation for studying altered gaseous environments. 1 88

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

CSF HCO3- increases more than plasma HCO3- in hypercapnia, and there are at least two sources for the CSF HCO3- increase--one derived from the simultaneous increase in plasma HCO3-, and the other, HCO3-formed from hydration of CO2 in the choroid plexus and glia and susceptible to inhibition by acetazolamide (J. Appl. Physiol. 38: 504-512, 1975). It was proposed that the H+ formed in the CNS in CO2 hydration is actively exchanged for plasma Na+ utilizing the Na-K ATPase pump. H+ transport from the CNS was therefore studied in four groups of dogs breathing 5% CO2 at constant VA for 4 h with repeated injections of saline, acetazolamide 5 mg/ml, ouabain 0.1 mg/ml, and acetazolamide and ouabain together into lateral cerebral ventricles. Arterial HCO3-increased 2.5 meq/l at 4 h of hypercapnia in all groups. CSF HCO3-increased 5.8 meq/l in the saline-injected animals, but it increased only about 2 meq/l and equaled plasma HCO3- rise in the other three groups. Therefore CNS HCO3- formation in hypercapnia can be blocked by inhibiting the CO2 hydration reaction with acetazolamide or by blocking H+ removal by inhibiting Na-K ATPase with ouabain. The data support the thesis of active H+ removal from the CNS in exchange for plasma Na+ in hypercapnia.
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PMID:H+ transport from CNS in hypercapnia and regulation of CSF [HCO3-]. 1 62

1. The regulation of cerebrospinal fluid (c.s.f.) bicarbonate concentration was studied using the cat choroid plexus isolated in a chamber in situ. 2. Decreases in plasma bicarbonate concentration caused relatively small changes in the c.s.f. bicarbonate concentration. 3. Alterations in c.s.f. bicarbonate concentration (c.s.f. HCO3-=9 or 28 m-equiv/l.) were countered by changes in the bicarbonate concentration of the fluid produced by the plexus or in the rate of bicarbonate transport which returned c.s.f. bicarbonate towards normal. 4. There was significant regulation of pH in the choroid plexus fluid during hypocapnia and hypercapnia. 5. Alterations of plasma acid-base status did not significantly alter the potential difference across the choroid plexus. However, the potential difference increased when c.s.f. bicarbonate was increased and decreased when c.s.f. bicarbonate was decreased. 6. The data indicate that the bicarbonate concentration in the c.s.f. is actively regulated by the choroid plexus during acid-base disturbances occurring either systemically or in the c.s.f.
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PMID:Regulation of cerebrospinal fluid bicarbonate by the cat choroid plexus. 1 33

Experiments were performed to determine the relative effects of a net extracellular-to-intracellular HCO3- flux and of elevated carbon dioxide tension (PCO2) on cellular acid-base regulation. Isolated rabbit hearts were perfused by recirculating a small volume of Ringer solution in which the PCO2 and the HCO3- concentration could be independently altered. Net HCO3- flux was assessed by the disappearance of HCO3- from perfusate. Between 40 and 100 Torr PCO2, a HCO3- flux into the cell occurs only when perfusate HCO3- concentration is increased. Therefore, by selective manipulation of perfusate HCO3- and PCO2 it is possible to induce hypercapnia with or without an accompanying HCO3- flux. When perfusate HCO3- concentration was increased from 20 to 36 mM, cellular HCO3- concentration increased from 22.5 +/- 0.8 to 26.1 +/- 1.0 mM at 40 Torr PCO2 and from 27.8 +/- 0.7 to 34.1 +/- 1.4 mM at 98 Torr PCO2. These increases can be accounted for by the amount of HCO3- that disappeared from the perfusate. The results suggest that most of the initial cell CO2 buffering is provided by the net HCO3- flux in addition to the passive physicochemical buffering.
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PMID:Contribution of a net transmembrane HCO3- flux to intracellular acid-base regulation. 2 30

Using a 14C-labeled DMO, 36Cl and 3H method, we have determined the in vivo buffering capacity of lung, kidney, heart, skeletal muscle, and extracellular fluid (ECF) of guinea pigs during hypercapnia (FICO2 = 0.15). After 1 days' exposureto 15% CO2, both the relative CO2 buffer values (delta HCO3/deltapH) and the "%pH regulation" were lung greater than kidney greater than heart greater than ECF greater than skeletal muscle. For lung tissue the intracellular pH was significantly decreased only during acute (8 h) hypercapnia and had completely returned to control values after 7 days with arterial PCO2 congruent to 122 Torr. Kidney and cardiac muscle also showed ca. 100% regulation of pH at 7 days, whereas skeletal muscle and ECF showed only 80 and 70% pH regulation, respectively. The results are discussed with respect to the important (and pH-dependent) metabolic functions of the lung and kidney.
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PMID:Regulation of intracellular pH in lungs and other tissues during hypercapnia. 2 85

The myocardial cell pH (pHi) observed during breathing of 0, 7.5, or 10% CO2 in air for 3 h was studied in rats with myocardial hypertrophy due to aortic stenosis and in sham-operated rats. The change in pHi during hypercapnia was significantly smaller in the rats with myocardial hypertrophy, with the apparent nonbicarbonate buffer value (delta [HCO3-]i/delta pHi) being almost three times that of the sham-operated rats. In vitro CO2 equilibrium of myocardial tissue homogenates showed no difference in nonbicarbonate buffer value between homogenates obtained from normal rats and from rats with myocardial hypertrophy. Therefore, it appears that the increased ability of the myocardial cell to regulate its pH during hypertrophy is not due to an increase in the cellular level of nonbicarbonate buffers, but seems to be related to a larger bicarbonate uptake by the myocardial cell during hypercapnia.
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PMID:Intracellular pH regulation of normal and hypertrophic rat myocardium. 4 27


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