Diffusion limitation and limitation by chemical reactions during alveolar-capillary transfer of oxygen-labeled CO2

Schuster, K.-D.

doi:10.1016/0034-5687(87)90003-x

Cited by 11 publications

(14 citation statements)

References 11 publications

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“…The slow phase is most likely due to the release of C 18 O 2 from various pulmonary dead spaces, which partly compensates for the elimination of C 18 O 2 from the proximal alveolar compartment. Thus, only the first 3 s of label decay reflect the kinetics of C 18 O 2 uptake by pulmonary‐capillary blood ( Schuster 1987). Therefore, the true P A C 18 O 2 values were obtained by subtracting the partial pressure of the remaining residues from the P A C 18 O 2 values measured during the fast phase.…”

Section: Resultsmentioning

confidence: 99%

Stratification does not limit O₂ uptake in rabbit lungs

Heller

Schuster

1998

Acta Physiologica Scandinavica

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This study was performed to assess the role of stratification, i.e. axial gas mixing deficit within alveolar space, in limiting alveolar gas exchange for oxygen. The single-breath method for varying breath-holding time with oxygen-labelled carbon dioxide, C18O2, was applied to 10 anaesthetized, paralysed and artificially ventilated rabbits. Alveolar partial pressure of C18O2 was analysed using respiratory mass spectrometry. Starting from residual volume, the lungs were rapidly inflated using 40 mL of indicator gas mixture (1% C18O2 in nitrogen). After executing breath-holding, the lungs were rapidly deflated. Pulmonary diffusing capacity of carbon monoxide was determined in the same way. On the basis of a serial compartment model, the lower limit of the stratificational conductance of oxygen was estimated, using the rate constant of C18O2 removal from alveolar space (4 s-1) and Graham's law. We found that the stratificational conductance in rabbits amounts to at least 13.5 mL mmHg-1 min-1. The pulmonary diffusing capacity of oxygen was calculated by multiplying the carbon monoxide diffusing capacity of rabbit lungs by a factor of 1.2, yielding a value of 0.77 mL mmHg-1 min-1. These results show that stratificational conductance is at least 17.5 times higher than pulmonary oxygen diffusing capacity, indicating that stratification does not limit oxygen uptake in rabbit lungs.

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Section: Resultsmentioning

confidence: 99%

Stratification does not limit O₂ uptake in rabbit lungs

Heller

Schuster

1998

Acta Physiologica Scandinavica

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“…In other words, 1/θ Vc is the resistance to CO 2 transfer provided by the chemical reactions of CO 2 and associated erythrocytic transport processes. The comparatively small contribution of the diffusion resistance across the alveolar-capillary barrier becomes manifest in the minimum estimate for D L, M , 1100 ml/mmHg/min, which compares with the overall diffusing capacity of the lung D L of 180 ml/mmHg/min (Schuster, 1987). Thus, D L, M makes up at most 1/6 of the total resistance for CO 2 exchange between lung and red cells.…”

Section: Protein Channels For Molecular Co2 In Membranes Of High Co2 mentioning

confidence: 96%

How does carbon dioxide permeate cell membranes? A discussion of concepts, results and methods

et al. 2014

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We review briefly how the thinking about the permeation of gases, especially CO2, across cell and artificial lipid membranes has evolved during the last 100 years. We then describe how the recent finding of a drastic effect of cholesterol on CO2 permeability of both biological and artificial membranes fundamentally alters the long-standing idea that CO2—as well as other gases—permeates all membranes with great ease. This requires revision of the widely accepted paradigm that membranes never offer a serious diffusion resistance to CO2 or other gases. Earlier observations of “CO2-impermeable membranes” can now be explained by the high cholesterol content of some membranes. Thus, cholesterol is a membrane component that nature can use to adapt membrane CO2 permeability to the functional needs of the cell. Since cholesterol serves many other cellular functions, it cannot be reduced indefinitely. We show, however, that cells that possess a high metabolic rate and/or a high rate of O2 and CO2 exchange, do require very high CO2 permeabilities that may not be achievable merely by reduction of membrane cholesterol. The article then discusses the alternative possibility of raising the CO2 permeability of a membrane by incorporating protein CO2 channels. The highly controversial issue of gas and CO2 channels is systematically and critically reviewed. It is concluded that a majority of the results considered to be reliable, is in favor of the concept of existence and functional relevance of protein gas channels. The effect of intracellular carbonic anhydrase, which has recently been proposed as an alternative mechanism to a membrane CO2 channel, is analysed quantitatively and the idea considered untenable. After a brief review of the knowledge on permeation of O2 and NO through membranes, we present a summary of the 18O method used to measure the CO2 permeability of membranes and discuss quantitatively critical questions that may be addressed to this method.

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“…An important challenge to gas exchange that affects acid-base balance is the fact that the transfer of CO 2 (mainly as bicarbonate) from erythrocytes during pulmonary capillary transit is (267), which also rapidly diffuses into the plasma and alveoli. The limitation at the lung has to do with the relatively slow rate of erythrocyte band 3 Cl − /HCO 3 − exchange and the need to rapidly evolve CO 2 at the lung.…”

Section: Erythrocyte Gas Exchangementioning

confidence: 99%

Effects of Gas Exchange on Acid‐Base Balance

Lindinger

Heigenhauser

2012

Comprehensive Physiology

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This paper describes the interactions between ventilation and acid-base balance under a variety of conditions including rest, exercise, altitude, pregnancy, and various muscle, respiratory, cardiac, and renal pathologies. We introduce the physicochemical approach to assessing acid-base status and demonstrate how this approach can be used to quantify the origins of acid-base disorders using examples from the literature. The relationships between chemoreceptor and metaboreceptor control of ventilation and acid-base balance summarized here for adults, youth, and in various pathological conditions. There is a dynamic interplay between disturbances in acid-base balance, that is, exercise, that affect ventilation as well as imposed or pathological disturbances of ventilation that affect acid-base balance. Interactions between ventilation and acid-base balance are highlighted for moderate- to high-intensity exercise, altitude, induced acidosis and alkalosis, pregnancy, obesity, and some pathological conditions. In many situations, complete acid-base data are lacking, indicating a need for further research aimed at elucidating mechanistic bases for relationships between alterations in acid-base state and the ventilatory responses.

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Diffusion limitation and limitation by chemical reactions during alveolar-capillary transfer of oxygen-labeled CO2

Cited by 11 publications

References 11 publications

Stratification does not limit O₂ uptake in rabbit lungs

Stratification does not limit O₂ uptake in rabbit lungs

How does carbon dioxide permeate cell membranes? A discussion of concepts, results and methods

Effects of Gas Exchange on Acid‐Base Balance

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Diffusion limitation and limitation by chemical reactions during alveolar-capillary transfer of oxygen-labeled CO2

Cited by 11 publications

References 11 publications

Stratification does not limit O2 uptake in rabbit lungs

Stratification does not limit O2 uptake in rabbit lungs

How does carbon dioxide permeate cell membranes? A discussion of concepts, results and methods

Effects of Gas Exchange on Acid‐Base Balance

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Product

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Stratification does not limit O₂ uptake in rabbit lungs

Stratification does not limit O₂ uptake in rabbit lungs