The ?in vivo? and ?in vitro? CO2-equilibration curves of blood during acute hypercapnia and hypocapnia

Böning, Dieter; Schweigart, U.; Nutz, V; Stegemann, Jürgen

doi:10.1007/bf00587799

Cited by 11 publications

(11 citation statements)

References 35 publications

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“…Before the stay at altitude the extracellular D[HCO À 3 ] á DpH A1 values were relatively high compared to previous results (BoÈ ning 1974;Brackett et al 1965;Siggaard-Andersen 1974). An increase in buer capacity might have been expected in this study because of the comparatively large initial Hb mass (but not [Hb]) in our well-trained subjects [881 44 g;BoÈ ning et al 1997] if the interstitial volume were to have been increased less than the blood volume compared to the untrained subjects.…”

Section: Extracellular Co 2 Storage and Bueringcontrasting

confidence: 54%

“…The constant slope over the whole pH range argues against a great in¯uence of the sequence. Other disturbing in¯uences such as equilibration time, arterial-mixed venous PCO 2 dierences and changes in cardiac output have been extensively discussed in previous papers including our own (BoÈ ning 1974;Cherniack and Longobardo 1970) and will not therefore be reconsidered here.…”

Section: Extracellular Co 2 Storage and Bueringmentioning

confidence: 94%

“…It has been shown that if the blood is titrated with CO 2 in vivo by hyperventilation and CO 2 rebreathing (in vivo CO 2 equilibration curve of blood), HCO À 3 is interchanged with the interstitial¯uid and an estimate of buering in the extracellular space is obtained (BoÈ ning 1974;Brackett et al 1965;Siggaard-Andersen 1974). Because of the Hamburger shift the erythrocytes supply the largest amount of buers for the protein-poor extracellular¯uid, whereas neither HCO À 3 nor H + transport across most tissue cell membranes have been found to play an important role during short experiments (Kemp et al 1994;Siggaard-Andersen 1974).…”

Section: Introductionmentioning

confidence: 97%

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Carbon dioxide storage and nonbicarbonate buffering in the human body before and after an Himalayan expedition

Böning

Maassen

Steinacker

et al. 1999

European Journal of Applied Physiology

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Before and 7-12 days after an Himalayan expedition CO2 equilibration curves were determined in the blood plasma of 12 mountaineers by in vitro and in vivo CO2 titration; in vivo osmolality changes (delta Osm x deltaPCO2(-1), deltaOsm x delta pH(-1), where PCO2 is the partial pressure of CO2) during the latter experiments yielded estimates of whole body CO2 storage. In vitro -delta[HCO3-] x delta pH(-1) [nonbicarbonate buffer capacity (beta) of blood] was increased 7 days after descent [before 31.3 (SEM 0.4) mmol x kgH2O(-1), after 38.3 (SEM 3.9) mmol x kgH2O(-1); P<0.05] resulting from an increased proportion of young erythrocytes; in additional experiments an augmented beta was found in young (low density cells) compared to old cells [<1.097 g x ml(-1): 0.216 (SEM 0.028) mmol x gHb(-1), >1.100 g x ml(-1): 0.145 (SEM 0.013) mmol x gHb(-1), where Hb is haemoglobin; P < 0.02]. In spite of increased Hb mass in vivo delta[CO2total] x deltaPCO2(-1) [0.192 (SEM 0.010) mmol x kgH2O(-1) x mmHg(-1)] and -delta[HCO3-] x delta pH(-1) [17.9 (SEM 1.0) mmol x kgH2O(-1)] as indicators of extracellular beta rose only slightly after altitude (7 days +16%, P<0.02; +7%, NS) because of haemodilution. The deltaOsm x deltaPCO2(-1) [0.230 (SEM 0.015) mosmol x kgH2O(-1) x mmHg(-1)] remained unchanged. Prealtitude differences in deltaOsm x delta pH(-1) between hypercapnia [-41 (SEM 5) mosmol x kgH2O(-1)] and hypocapnia [-20 (SEM 3) mosmol x kgH2O(-1); P<0.01] disappeared temporarily after return since the former slope was reduced. The high value during hypercapnia before ascent probably resulted from mechanisms stabilizing intracellular pH during moderate hypercapnia which were attenuated after descent.

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Section: Extracellular Co 2 Storage and Bueringcontrasting

confidence: 54%

Section: Extracellular Co 2 Storage and Bueringmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 97%

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Carbon dioxide storage and nonbicarbonate buffering in the human body before and after an Himalayan expedition

Böning

Maassen

Steinacker

et al. 1999

European Journal of Applied Physiology

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“…Because of this long known effect, ABE as well as standard bicarbonate of blood sampled during acute respiratory acidosis are lowered (e.g. Beecher and Murphy 1950;Dell and Winters 1970;Bö ning et al 1974;Siggaard-Andersen 1974).…”

Section: Introductionmentioning

confidence: 98%

Causes of differences in exercise-induced changes of base excess and blood lactate

et al. 2006

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It has been concluded from comparisons of base excess (BE) and lactic acid (La) concentration changes in blood during exercise-induced acidosis that more H+ than La- leave the muscle and enter interstitial fluid and blood. To examine this, we performed incremental cycle tests in 13 untrained males and measured acid-base status and [La] in arterialized blood, plasma, and red cells until 21 min after exhaustion. The decrease of actual BE (-deltaABE) was 2.2 +/- 0.5 (SEM) mmol l(-1) larger than the increase of [La]blood at exhaustion, and the difference rose to 4.8 +/- 0.5 mmol l(-1) during the first minutes of recovery. The decrease of standard BE (SBE), a measure of mean BE of interstitial fluid (if) and blood, however, was smaller than the increase of [La] in the corresponding volume (delta[La](if+blood)) during exercise and only slightly larger during recovery. The discrepancy between -deltaABE and delta[La]blood mainly results from the Donnan effect hindering the rise of [La]erythrocyte to equal values like [La]plasma. The changing Donnan effect during acidosis causes that Cl- from the interstitial fluid enter plasma and erythrocytes in exchange for HCO3(-). A corresponding amount of La- remains outside the blood. SBE is not influenced by ion shifts among these compartments and therefore is a rather exact measure of acid movements across tissue cell membranes, but changes have been compared previously to delta[La]blood instead to delta[La](if+blood). When performing correct comparisons and considering Cl-/HCO3(-) exchange between erythrocytes and extracellular fluid, neither the use of deltaABE nor of deltaSBE provides evidence for differences in H+ and La- transport across the tissue cell membranes.

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“…In contrast the amount of non-bicarbonate buffers in the extracellular space (mainly plasma and interstitial proteins, phosphates) is low, but red cell buffers, especially hemoglobin (Hb), are available to this compartment because of the HCO 3 -versus Cl -exchange across the erythrocytic membrane (Hamburger shift). Extracellular b nbi at rest amounts to 10-17 mmol l -1 per pH unit and thus moderately exceeds that of blood, which was diluted 3 times by interstitial fluid (9 mmol l -1 , Böning 1974). This quantity can be measured by in vivo titration with CO 2 in hypercapnia-hypocapnia experiments (e.g.…”

Section: Introductionmentioning

confidence: 98%

Extracellular bicarbonate and non-bicarbonate buffering against lactic acid during and after exercise

et al. 2007

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Defense of extracellular pH constancy against lactic acidosis can be estimated from changes (Delta) in lactic acid ([La]), [HCO(3)(-)], pH and PCO(2) in blood plasma because it is equilibrated with the interstitial fluid. These quantities were measured in earlobe blood during and after incremental bicycle exercise in 13 untrained (UT) and 21 endurance-trained (TR) males to find out if acute and chronic exercise influence the defense. During exercise the capacity of non-bicarbonate buffers (beta(nbi) = -Delta[La] . DeltapH(-1) - Delta[HCO(3)(-)] . DeltapH(-1)) available for the extracellular fluid (mainly hemoglobin, dissolved proteins and phosphates) amounted to 32 +/- 2(SEM) and 20 +/- 2 mmol l(-1) in UT and TR, respectively (P < 0.02). During recovery beta(nbi) decreased to 14 (UT) and 12(TR) mmol l(-1) (both P < 0.001) corresponding to values previously found at rest by in vivo CO(2) titration. Bicarbonate buffering (beta(bi)) amounted to 44-48 mmol l(-1) during and after exercise. The large exercise beta(nbi) seems to be mainly caused by an increasing concentration of all buffers due to shrinking of the extracellular volume, exchange of small amounts of HCO(3)(-) or H(+) with cells and delayed HCO(3)(-) equilibration between plasma and interstitial fluid. Increase of [HCO(3)(-)] during titration by these mechanisms augments total beta and thus the calculated beta(nbi) more than beta(bi) because it reduces DeltapH and Delta[HCO(3)(-)] at constant Delta[La]. The smaller rise in exercise beta(nbi) in TR than UT may be caused by an increased extracellular volume and an improved exchange of La(-), HCO(3)(-) and H(+) between trained muscles and blood.

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The ?in vivo? and ?in vitro? CO2-equilibration curves of blood during acute hypercapnia and hypocapnia

Cited by 11 publications

References 35 publications

Carbon dioxide storage and nonbicarbonate buffering in the human body before and after an Himalayan expedition

Carbon dioxide storage and nonbicarbonate buffering in the human body before and after an Himalayan expedition

Causes of differences in exercise-induced changes of base excess and blood lactate

Extracellular bicarbonate and non-bicarbonate buffering against lactic acid during and after exercise

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