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K D Schuster

Publications and source records attributed to K D Schuster.

28 records · Page 2Linked to original sources
PubMed1990

Cardiogenic oscillations of He and SF6 in expired gas in dogs.

Quantitative analysis of cardiogenic oscillations of He and SF6 during airway and venous loading demonstrated that both VA/Q and VA/VA inequalities were involved in the lung gas inhomogeneity producing cardiac oscillations in the expirogram. Both inequalities were coupled in such a manner that low VA/Q units had high VA/VA. The oscillations were modified in conducting airways where SF6 oscillations were attenuated more than He oscillations, probably by laminar Taylor dispersion.

Animals↗
PubMed1990

Assessment of stratified inhomogeneity within distal alveolar space with respect to oxygen uptake.

Investigations were made as to whether or not there is a limitation of oxygen transport by stratified inhomogeneity in distal alveolar gas. Experiments were performed on 2 subjects. Single breath manoeuvres were carried out with similar phases of inspiration and expiration but varying breath-hold times. The inspiratory gas contained a small amount of oxygen labeled carbon dioxide, C18O2. End-expiratory gas was analysed on its residual C18O2 partial pressure by mass spectrometry. For evaluating a stratificational conductance, compartment model analysis was applied on the breath-hold data. Stratificational conductance has been found to be higher than 553 ml.mmHg-1. min-1. When transferred to oxygen transport, this means that stratificational conductance is more than 10 times higher than oxygen diffusing capacity. It can be concluded that (i) stratified inhomogeneity in distal alveolar space does not exhibit a limiting factor of oxygen uptake in lungs, (ii) a contribution of stratificational effects to sloping alveolar plateau is expected to be of minor importance.

Adult↗
PubMed1990

Pulmonary diffusing capacities for nitric oxide and carbon monoxide determined by rebreathing in dogs.

Pulmonary diffusing capacities (DL) of NO and CO were determined simultaneously from rebreathing equilibration kinetics in anesthetized paralyzed supine dogs (mean body wt 20 kg) after denitrogenation (replacement of N2 by Ar). During rebreathing the dogs were ventilated in closed circuit with a gas mixture containing 0.06% NO, 0.06% 13C18O, and 1% He in Ar for 15 s, with tidal volume of 0.5 liter and frequency of 60/min. The partial pressures of NO, 13C18O, 16O18O, N2, Ar, CO2, and He in the trachea were continuously analyzed by mass spectrometry. Measurements were performed at various O2 levels characterized by the mean end-expired PO2 during rebreathing (PE'O2). In control conditions ("normoxia," PE'O2 = 67 +/- 8 Torr) the following mean +/- SD values were obtained (in ml.min-1.Torr-1): DLNO = 52.4 +/- 11.0 and DLCO = 15.4 +/- 2.9. In hypoxia (PE'O2 = 24 +/- 7 Torr) DLNO increased by 11 +/- 8% and DLCO by 19 +/- 10%, and in hyperoxia (PE'O2 = 390 +/- 26 Torr) DLNO decreased to 87 +/- 3% and DLCO to 56 +/- 8% with respect to values in normoxia. DLNO/DLCO of 3.24 +/- 0.06 (hypoxia), 3.38 +/- 0.31 (normoxia), and 5.54 +/- 1.04 (hyperoxia) were significantly higher than the NO/CO Krogh diffusion constant ratio (1.92) predicted for simple diffusion through aqueous layers. With increasing O2 uptake elicited by 2,4-dinitrophenol, DLNO and DLCO increased and DLNO/DLCO remained close to unchanged. The results suggest that the combined effects of diffusion and chemical reaction with hemoglobin limit alveolar-capillary transport of CO. If it is assumed that reaction kinetics of NO with hemoglobin (known to be extremely fast) are not rate limiting for NO uptake, the contribution of the slow chemical reaction with hemoglobin to the total CO uptake resistance (= 1/DLCO) was estimated to be 38% in hypoxia, 41% in normoxia, and 64% in hyperoxia. The various factors expected to restrict the validity of this analysis are discussed, in particular the effects of functional inhomogeneity.

2,4-Dinitrophenol↗
PubMed1990

Alveolar slope and dead space of He and SF6 in dogs: comparison of airway and venous loading.

Series (Fowler) dead space (VD) and slope of the alveolar plateau of two inert gases (He and SF6) with similar blood-gas partition coefficients (approximately 0.01) but different diffusivities were analyzed in 10 anesthetized paralyzed mechanically ventilated dogs (mean body wt 20 kg). Single-breath constant-flow expirograms were simultaneously recorded in two conditions: 1) after equilibration of lung gas with the inert gases at tracer concentrations [airway loading (AL)] and 2) during steady-state elimination of the inert gases continuously introduced into venous blood by a membrane oxygenator and partial arteriovenous bypass [venous loading (VL)]. VD was consistently larger for SF6 than for He, but there was no difference between AL and VL. The relative alveolar slope, defined as increment of partial pressure per increment of expired volume and normalized to mixed expired-inspired partial pressure difference, was larger by a factor of two in VL than in AL for both He and SF6. The He-to-SF6 ratio of relative alveolar slope was generally smaller than unity in both VL and AL. Whereas unequal ventilation-volume distribution combined with sequential emptying of parallel lung regions appears to be responsible for the sloping alveolar plateau during AL, the steeper slope during VL is attributed to the combined effects of continuing gas exchange and ventilation-perfusion inequality coupled with sequential emptying. The differences between He and SF6 point at the contributing role of diffusion-dependent mechanisms in intrapulmonary gas mixing.

Administration, Inhalation↗
PubMed1990

Cardiogenic oscillations in He and SF6 expirograms during airway and venous loading.

Cardiogenic oscillations in the expired partial pressure profiles of two inert gases (He and SF6) were monitored in seven anesthetized paralyzed mechanically ventilated dogs. He and SF6 were administered either intravenously by a membrane oxygenator and partial arteriovenous bypass [venous loading (VL)] or by washin into lung gas [airway loading (AL)]. The single-breath expirograms obtained during constant-flow expiration after inspiration of test gas-free air displayed distinct and regular cardiogenic oscillations. The relative oscillation amplitude (ROA), calculated as oscillation amplitude divided by mixed expired-inspired partial pressure difference, was in the range of 1-8%. The ROA for both He and SF6 was approximately 4.2 times higher in VL than in AL, which indicated that among lung units that emptied sequentially in the cardiac cycle, the effects of alveolar ventilation-perfusion (VA/Q) inequality were more pronounced than those of alveolar ventilation-alveolar volume (VA/VA) inequality. In AL, He and SF6 oscillations were 180 degrees out of phase compared with CO2 and O2 oscillations and with He and SF6 oscillations in VL, which suggests that regions with low VA/VA had high VA/Q and very low Q/VA. The ROA was practically unaffected by breath holding in both AL and VL, which indicates that there was little diffusive or convective (cardiogenic) mixing between the lung units that were responsible for cardiogenic oscillations. The ROA was consistently higher for He than for SF6, and the He-to-SF6 ratio was independent of route of test gas loading, averaging 1.6 in both AL and VL. This result may be explained by laminar Taylor dispersion, whereby oscillations generated in peripheral lung regions are dissipated in inverse proportion to diffusion coefficient during transit through the proximal (larger) airways.

Administration, Inhalation↗
PubMed1989

The overall fractionation effect of isotopic oxygen molecules during oxygen transport and utilization in humans.

The aim of the study was to clarify (1) whether fractionation effects of isotopic oxygen molecules due to respiratory processes can be neglected in tracer studies, (2) whether additional information about respiratory processes can be obtained from measuring isotope fractionations. Experiments were performed on 7 healthy humans at rest. Samples were taken from inspiratory and expiratory gas. After having removed the carbon dioxide from the samples, the oxygen was completely burnt with graphite to CO2, and the 16O18O/16O2 ratio of the CO2 generated was analysed by mass spectrometry. The 16O18O/16O2 ratio of the expiratory gas was 0.21 +/- 0.07% greater than that of the inspiratory air. The overall rate constant for uptake, subsequent transport and utilization was higher for 16O2 by 0.91 +/- 0.24% than for 16O18O. These results together with model calculations including data from literature suggest: (1) the fractionation effects between 16O18O and 16O2 as well as between 18O2 and 16O2 are small enough for both isotopic species to be considered appropriate labels in the investigation of respiratory processes, (2) the effect measured could be due to limitations of oxygen transport by utilization, (3) additional processes such as the reaction of oxygen with hemoglobin could be involved in forming the overall fractionation effect.

Carbon Dioxide↗
PubMed1989

Fractionation of oxygen isotopes due to equilibration of oxygen with hemoglobin.

The aim of the study was to answer the question as to whether the chemical reaction of oxygen with hemoglobin exhibits a source of isotopic fractionation, which could be of significance in forming the overall fractionation effect of respiration recently determined in man. Investigations were performed on bovine hemoglobin solutions adjusted to normal values of Hb concentration and pH. After degassing in vacuo, the hemoglobin solution was equilibrated in a closed system with pure oxygen of suitable pressure so that oxygen saturation levels of 30, 50 and 100% were achieved. After complete equilibration, isotope analysis of oxygen by mass spectrometry resulted in 16O18O/16O2 ratios which were 0.35 +/- 0.02% lower in the oxygen bound to hemoglobin than that of the gas phase during all levels of oxygenation. Model calculations suggest the following: (1) the fractionation during oxygen uptake in the lung at rest is primarily determined by the reaction with hemoglobin, (2) the overall fractionation effect of respiration can be explained as due to single effects of the constituent processes when assuming the oxygen transport to be limited by utilization.

Animals↗
PubMed1987

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

A major difficulty in the measurement of carbon dioxide diffusing capacity is the development of significant CO2 back pressure within the capillary. The use of oxygen-labeled CO2 limits this back pressure due to rapid dilution of the label into the water pool by isotopic exchange. We demonstrated the use of C16O18O to measure DCO2 (Schuster, 1985). A major question from that study is whether the isotope measures a true membrane diffusing capacity or is limited by back reaction. In this study we examine the diffusing capacity of doubly 18O-labeled carbon dioxide, C18O2, a species in which the kinetics of isotopic exchange in pulmonary blood is higher than that of C16O18O. Eighteen single breath experiments were performed on two resting male subjects whose CO2-transfer-kinetics was previously studied with C16O18O (Schuster, 1985). Following expiration to residual volume the subjects inspired a gas mixture containing 20% O2 and 1.5-2.6% C18O2. After holding their breath for 0.4-17 sec they exhaled into a tube and the end-expired gas was analysed by mass spectrometry. The time course of the C18O2 disappearance from alveolar gas showed a biexponential characteristic as that which had been measured with C16O18O, but C18O2 disappeared faster. The mean value of the diffusing capacity of C18O2 amounts to 1102 ml mmHg-1 X min-1. It is 228 +/- 163 ml mmHg-1 X min-1 greater than that of C16O18O. This significant difference suggests that: DC16O18O is limited in part by isotopic exchange reactions; the observed DC18O2 may be taken as a new lower limit for DMCO2, higher than values established from other techniques; the decarboxylation of bicarbonate in red cells is not a rate limiting step for CO2 exchange.

Adult↗
PubMed1985

Kinetics of pulmonary CO2 transfer studied by using labeled carbon dioxide C16O18O.

The kinetics of alveolar-capillary CO2 transfer was investigated, using 18O-labeled carbon dioxide (C16O18O), in 21 experiments on 2 resting human subjects. Single-breath experiments were performed. After the subjects expired to residual volume, they inspired a gas mixture containing 20% O2 and 2.8% CO2 - a quarter of CO2 was labeled with 18O. The breath-hold time ranged between 0.5 and 20 sec. After expiration the gas mixture was analysed by mass spectrometry. The C16O18O concentration of the end-expiratory gas decreased with the increasing breath-hold time. The relationship of both showed a biexponential characteristic with the two time constants 0.4 and 16 sec. The lower time constant characterizes the CO2 transfer from the alveolar space to the capillary blood, as well as the isotopic equilibration of the 18O within the blood. The higher time constant could result from small admixtures of the label from the dead spaces or the lung tissues. The diffusing capacity of C16O18O was calculated by using the first part of the indicator clearance curve. The derived mean value of 862 ml X mm Hg-1 X min-1 is considered to be a lower limit of the 'membrane diffusing capacity' for CO2 (DMCO2).

Adult↗