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

Arterial blood acid-base status of unanesthetized, unrestrained nutria was studied during exposure to 5, 10 and 14.5% CO2 for 6 hr. Control values, pH = 7.426 +/- 0.037, PaCo2 = 36.5 +/- 3.1 mmHg and [HCO-3] = 24.3 +/- 2.5 mM/1 (n = 24), are within the normal range reported for other mammals. Values after 6 hr of exposure to 10% CO2 were: pH = 7.355 +/- 0.043, PaCO2 = 71.0 +/- 3.6 mmHg and [HCO-3] = 38.0 +/- 4.1 mM/l (n = 5). Arterial blood buffer slopes, obtained from the in vitro titration curve, did not show any pattern of adaptation to hypercapnia. Whole body buffer slopes, calculated from the in vivo CO2 titration curve, showed significantly higher values for the nutria than for the rat, dog and man, under comparable conditions [beta(delta HCO-3/delta pH)] = 57.0 slykes for nutria, 32.6 for rat and 11.8 for man. delta H+/delta PaCO2 = 0.38. mM/l/mmHg for nutria, 0.55 for rat and 0.76 for man. The results suggest that the nutria possesses an efficient metabolic mechanism for regulation of pH level during exposure to hypercapnic conditions.
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PMID:Adaptations to hypercapnic conditions in the nutria (Myocastor coypus)--in vivo and in vitro CO2 titration curves. 613 14

Disorders of systemic acid-base balance have recently been shown to markedly alter intestinal electrolyte transport. These studies were based on earlier acid balance studies in humans and animals, data suggesting the presence of intestinal mucosal Na+-H+ and Cl-HCO-3 exchange processes and the reported effects of acid-base variables on other epithelia. In vivo studies have shown that intestinal net sodium and chloride absorption is markedly affected by systemic pH and carbon dioxide tension (Pco2). Specifically, systemic acidemia (in the rat ileum) and hypercapnia (in the rat colon) increase sodium and chloride absorption, while alkalemia and hypocapnia decrease absorption. In addition, net bicarbonate secretion (in both segments) varies directly with the plasma HCO3 concentration. The rabbit ileum has been studied both in vivo and in vitro and is affected in a similar way. The rat jejunum and rabbit distal colon and gallbladder do not respond to changes in blood pH and Pco2, consistent with the apparent absence of a mucosal Na+-H+ exchange process in these segments. Evidence suggests important roles for cellular carbonic anhydrase activity and the intracellular concentrations of hydrogen, bicarbonate, and calcium ions and calcium-calmodulin in mediating or modulating the effects of the systemic acid-base disorders. In addition, systemic pH may alter the effects of the neural and humoral mediators of intestinal transport.
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PMID:Systemic acid-base disorders and intestinal electrolyte transport. 633 Nov 93

The aquatic urodeles Ambystoma tigrinum and Necturus maculosus responded to hypercapnia quite differently. A. tigrinum, after 2-h exposure to 22 Torr partial pressure of CO2 (PCO2), decreased arterial pH (pHa) from 7.85 to 7.32 and increased arterial pressure of CO2 (PaCO2) to 26 Torr. Plasma [HCO-3] [( HCO-3]pl) remained constant at about 17 mM. Prolonged exposure (24 h) led to a 26% extracellular compensation as pHa rose to 7.46 while [HCO-3]pl increased to 24 mM. Plasma [K+] increased and [Cl-] decreased while [Na+] remained unchanged. Recovery in normocapnic water reversed these changes. N. maculosus did not display similar compensatory changes. Two-hour exposure to 17 Torr PCO2 resulted in a decline of pHa from 7.66 to 7.24, which was not compensated (pHa = 7.19) after 24 h. There were no significant changes in plasma [Na+], [K+], [Cl-], or [HCO-3]. The pHa decline reversed after recovery in normocapnic water, however. The fact that compensation for hypercapnic in A. tigrinum was accompanied by changes in Cl- and K+ concentrations may indicate the participation of epithelial transport mechanisms involving these ions in acid-base balance.
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PMID:Acid-base and ionic balance in Ambystoma tigrinum and Necturus maculosus during hypercapnia. 641 88

Resting awake dogs breathing CO2 lower body temperature and such a change is reported to decrease the ventilatory response to CO2. Therefore, in 6 awake dogs the ventilatory response to CO2, obtained while body temperature was allowed to decrease spontaneously, was compared to the response obtained during warming of their body surface in an attempt to prevent the fall in temperature during hypercapnia. During warming, rectal temperature was maintained 0.5 to 0.7 degrees C higher than when TR was allowed to fall. In warm studies arterial [HCO-3]a was decreased relative to PaCO2 whereas there was a surprisingly large storage of CO2, 17.3 ml CO2/kg . Torr PaCO2. Ventilation was comparable in the dogs during air control of both experiments and before body warming was initiated. Subsequently, there was no consistent effect of warming on either the slope or threshold of the ventilatory response to CO2 with respect to either PaCO2 or pHa. Therefore, producing a higher and more 'normothermic' TR during hypercapnia in awake dogs had no definitive effect on chemical control of breathing.
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PMID:The effect of body warming on the ventilatory response to CO2 in the awake dog. 681 54

The relative importance of changes in extracellular fluid (ECF) pH in mediating increases in cerebral blood flow (CBF) during hypoxia and hypercapnia was assessed by varying [HCO(-3)]ECF in pentobarbital-anesthetized dogs. Blood flow to one caudate nucleus (CNBF) that was bathed by cerebrospinal fluid (CSF) of varied [HCO(-3)] was compared with CNBF (measured by radiolabeled microspheres) on the contralateral side, which received a normal-[HCO(-3)]CSF perfusate. Raising [HCO(-3)]CSF from 25 to 60 meq/l for 150 min lowered CNBF by 16% and suppressed the slope of cNBF response to hypercapnia by 61% but suppressed the slope of CNBF response to hypoxia significantly less (22%). Lowering [HCO(-3)]CSF to 8 meq/l increased CNBF by 71% and augmented the response to hypercapnia by 126% but did not alter the slope of the response to hypoxia. These data indicate that changes in [H+]ECF can account for the increased CBF during hypercapnia but not for the entire hypoxic response. The increase in lactic acid production that would be necessary to solely account for the increase in CBF during hypoxia is much greater than what has been reported in the literature.
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PMID:Bicarbonate ion modulation of cerebral blood flow during hypoxia and hypercapnia. 709 77

Pathophysiologic ecologic and therapeutic study was made on respiratory disturbances, especially on hypercapnia in patients with lung tuberculosis. 1) Of all in-patients (497 cases), 192 (38.6%) had respiratory disturbances, among which 70 cases (14.1%) exhibited hypercapnia. 2) Of these hypercapnic patients, about one-third (31.4%) were after thoracoplastic surgery, the main disturbances being restrictive in nature. In the half of non-operative cases, obstruction and inadequate gas mixing were the main cause for hypercapnia. 3) Critical values for inducing hypercapnia were % VC 45 for patients with restrictive disturbances and FEV1-0%/expected VC 40 for hypercapnic patients. 4) Significant band in the PaCO2 similar to (HCO-3) regression chart in patients (20 cases) with chronic stable hypercapnia showed a linear relationship with an increasing PaCO2, given by an equation, (HCO-3)p = 7.7 + 0.43 PaCO2 (PaCO2 45 -- 113 mmHg, SD = +/- 1.2, r = 0.99). Twelve percent of the unstable patients (100 cases) showed an alkalosis (pH greater than 7.45) over the range above 45 mmHg of PaCO2. 5) Even in patients with normal pH values, administered HCO-3 was estimated to move into the intracellular or interstitial fluid. 6) Increase in oxygen consumption was greater with increasing ventilation volume in hypercapneic patients. Even in these patients, voluntary or drug-induced hyperventilation caused a decrease in PaCO2, resulting in an amelioration of suppressed respiration under oxygen or even pethidine HCl administration. Discussion was made on the usefulness of these therapies on patients with hypercapnia.
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PMID:[Studies on hypercapnia in patients with lung tuberculosis (author's transl)]. 723 19

Extracellular acidosis has been demonstrated to play a key role in the process of metabolic depression under long-term environmental stress, exemplified in the marine invertebrate Sipunculus nudus. These findings led to the hypothesis that acid-base regulation is associated with a visible cost depending on the rate and mode of H(+)-equivalent ion exchange. To test this hypothesis, the effects of different ion-transport inhibitors on the rate of pH recovery during hypercapnia, on energy turnover and on steady-state acid-base variables were studied in isolated body wall musculature of the marine worm Sipunculus nudus under control conditions (pHe 7.90) and during steady-state extracellular acidosis (pHe 7.50 or 7.20) by in vivo (31)P-NMR and oxygen consumption analyses. During acute hypercapnia (2 % CO(2)), recovery of pHi was delayed at pHe 7.5 compared with pHe 7.9. Inhibition of the Na(+)/H(+)-exchanger by 5-(N,N-dimethyl)-amiloride (DMA) at pHe 7.5 delayed recovery even further. This effect was much smaller at pHe 7.9. Inhibition of anion exchange by the addition of the transport inhibitor 4, 4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS) prevented pH recovery at pHe 7.5 and delayed recovery at pHe 7.9, in accordance with an effect on Na(+)-dependent Cl(-)/HCO(3)(-) exchange. The effects of ouabain, DIDS and DMA on metabolic rate were reduced at low pHe, thereby supporting the conclusion that acidosis caused the ATP demand of Na(+)/K(+)-ATPase to fall. This reduction occurred via an inhibiting effect on both Na(+)/H(+)- and Na(+)-dependent Cl(-)/HCO(3)(-) (i.e. Na(+)/H(+)/Cl(-)/HCO(3)(-)) exchange in accordance with a reduction in the ATP demand for acid-base regulation during metabolic depression. Considering the ATP stoichiometries of the two exchangers, metabolic depression may be supported by the predominant use of Na(+)/H(+)/Cl(-)/HCO(3)(-) exchange under conditions of extracellular acidosis.
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PMID:Modulation of the cost of pHi regulation during metabolic depression: a (31)P-NMR study in invertebrate (Sipunculus nudus) isolated muscle. 1090 56

The role of changes of intracellular pH (pH(i)) as the proximal signal in central chemosensitive neurons has been studied. pH(i) recovery from acidification is mediated by Na(+)/H(+) exchange in all medullary neurons and pH(i) recovery from alkalinization is mediated by Cl(-)/HCO(3)(-) exchange in most medullary neurons. These exchangers are more sensitive to inhibition by changes in extracellular pH (pH(o)) in neurons from chemosensitive regions compared to those from nonchemosensitive regions. Thus, neurons from chemosensitive regions exhibit a maintained intracellular acidification in response to hypercapnic acidosis but they show pH(i) recovery in response to isohydric hypercapnia. A similar pattern of pH(i) response is seen in other CO(2)/H(+)-responsive cells, including glomus cells, sour taste receptor cells, and chemosensitive neurons from snails, suggesting that a maintained fall of pH(i) is a common feature of the proximal signal in all CO(2)/H(+)-sensitive cells. To further evaluate the potential role of pH(i) changes as proximal signals for chemosensitive neurons, studies must be done to: determine why a lack of pH(i) recovery from hypercapnic acidosis is seen in some nonchemosensitive neurons; establish a correlation between hypercapnia-induced changes of pH(i) and membrane potential (V(m)); compare the hypercapnia-induced pH(i) changes seen in neuronal cell bodies with those in dendritic processes; understand why the V(m) response to hypercapnia of many chemosensitive neurons is washed out when using whole cell patch pipettes; and employ knock out mice to investigate the role of certain proteins in the CO(2)/H(+) response of chemosensitive neurons.
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PMID:Intracellular pH regulation of neurons in chemosensitive and nonchemosensitive areas of brain slices. 1173 45

The exercising Thoroughbred horse (TB) is capable of exceptional cardiopulmonary performance. However, because the ventilatory equivalent for O2 (VE/VO2) does not increase above the gas exchange threshold (Tge), hypercapnia and hypoxemia accompany intense exercise in the TB compared with humans, in whom VE/VO2 increases during supra-Tge work, which both removes the CO2 produced by the HCO buffering of lactic acid and prevents arterial partial pressure of CO2 (PaCO2) from rising. We used breath-by-breath techniques to analyze the relationship between CO2 output (VCO2) and VO2 [V-slope lactate threshold (LT) estimation] during an incremental test to fatigue (7 to approximately 15 m/s; 1 m x s(-1) x min(-1)) in six TB. Peak blood lactate increased to 29.2 +/- 1.9 mM/l. However, as neither VE/VO2 nor VE/VCO2 increased, PaCO2 increased to 56.6 +/- 2.3 Torr at peak VO2 (VO2 max). Despite the presence of a relative hypoventilation (i.e., no increase in VE/VO2 or VE/VCO2), a distinct Tge was evidenced at 62.6 +/- 2.7% VO2 max. Tge occurred at a significantly higher (P < 0.05) percentage of VO2 max than the lactate (45.1 +/- 5.0%) or pH (47.4 +/- 6.6%) but not the bicarbonate (65.3 +/- 6.6%) threshold. In addition, PaCO2 was elevated significantly only at a workload > Tge. Thus, in marked contrast to healthy humans, pronounced V-slope (increase VCO2/VO2) behavior occurs in TB concomitant with elevated PaCO2 and without evidence of a ventilatory threshold.
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PMID:Mechanistic basis for the gas exchange threshold in Thoroughbred horses. 1189 16

Increased CO(2) partial pressures (hypercapnia) as well as hypoxia are natural features of marine environments like the intertidal zone. Nevertheless little is known about the specific effects of CO(2) on metabolism, except for the well-described effects on acid-base variables and regulation. Accordingly, the sediment-dwelling worm Sipunculus nudus was used as an experimental model to investigate the correlation of acid-base-induced metabolic depression and protein/amino acid catabolism, by determining the rates of oxygen consumption, ammonia excretion and O/N ratios in non-perfused preparations of body wall musculature at various levels of extra- and intracellular pH, P(CO(2)) and [HCO(3)(-)]. A decrease in extracellular pH from control level (7.9) to 6.7 caused a reduction in aerobic metabolic rate of both normocapnic and hypercapnic tissues by 40-45 %. O/N ratios of 4.0-4.5 under control conditions indicate that amino acid catabolism meets the largest fraction of aerobic energy demand. A significant 10-15 % drop in ammonia excretion, a simultaneous reduction of O/N ratios and a transient accumulation of intracellular bicarbonate during transition to extreme acidosis suggest a reduction in net amino acid catabolism and a shift in the selection of amino acids used, favouring monoamino dicarboxylic acids and their amines (asparagine, glutamine, aspartic and glutamic acids). A drop in intracellular pH was identified as mediating this effect. In conclusion, the present data provide evidence for a regulatory role of intracellular pH in the selection of amino acids used by catabolism.
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PMID:Changes in metabolic rate and N excretion in the marine invertebrate Sipunculus nudus under conditions of environmental hypercapnia: identifying effective acid-base variables. 1191 74


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