Adaptation of Respiratory Mass Spectrometer to Continuous Recording of Abundance Ratios of Stable Oxygen Isotopes

Acta Physiologica Scandinavica

Schuster

1998

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.

Section: Methodsmentioning

confidence: 99%

Stratification does not limit O₂ uptake in rabbit lungs

Acta Physiologica Scandinavica

Schuster

1998

“…After having completed each single-breath manoeuvre, the animals were ventilated with room air again and the dried alveolar gas sample was aspirated into the inlet system of the mass spectrometer (2-m heated steel inlet capillary, gas flow 5 ml/min). The relevant gases were detected at the relevant mass-to-charge ratios (30 for NO + and 40 for Ar + ), exploiting the reference gas technique [18] to avoid drift errors and cross-talk effects. The signal-to-noise ratios were 660:1 at 0.05% NO and 3200:1 at 0.934% Ar.…”

Section: Experimental Designmentioning

confidence: 99%

How to calculate the single-breath nitric oxide diffusing capacity in rabbits

Pfl�gers Archiv European Journal of Physiology

Schuster

2000

Self Cite

Nitric oxide (NO) is a novel indicator gas for investigating alveolar capillary gas exchange conditions. In clinical practice, pulmonary gas uptake is determined by measuring the single-breath diffusing capacity (DL,NO). Different algorithms are employed to calculate DL,NO. To compare the accuracy of those most commonly used, we performed single-breath experiments on 12 artificially ventilated rabbits. In each animal four manoeuvres, executing breath-holds of 2, 4, 6 and 8 s, were carried out. In each case we administered 55 ml of an indicator gas mixture containing 0.05% NO. Alveolar gas was analysed by respiratory mass spectrometry. The two algorithms for calculating DL,NO based on the conventional solution of the breath-holding equation [Ogilvie et al. (1957) J Clin Invest 36:1-17 and Jones and Meade (1961) Q J Exp Physiol 46:131-143], were compared with the three-equation technique [Graham et al. (1980) IEEE Trans Biomed Eng 27:221-227] as the reference. The deviation between DL,NO calculated from the conventional methods and the reference decreased linearly with increasing duration of NO uptake (deltat). The mean deviations declined from 16.6% (Jones and Meade) or 7.7% (Ogilvie) at deltat=4 s to 5.7% (Jones and Meade) or 2.4% (Ogilvie) at deltat=10 s. The larger mean values are due to the conventional solution where three-tenths of the inflation time is subtracted from deltat. These findings qualify the common prediction that the latter method yields DL,NO values of the highest accuracy. We therefore recommend Ogilvie's procedure if the three-equation technique cannot be employed.

“…We analysed the alveolar partial pressure of nitric oxide (P A NO) within the end-tidal portion of the alveolar gas sample. In order to reduce side-effects and drift errors, the sample gas was repeatedly compared with a reference gas only differing in the NO content (Schuster et al 1979). We calculated D L NO values as previously introduced by Schuster (1985).…”

Section: Single-breath Diffusing Capacity For Nitric Oxidementioning

confidence: 99%

Effect of inhaled nitric oxide on endotoxin‐induced hypoxaemia in rabbits

Acta Physiologica Scandinavica

Hoffmann

Schobersberger

et al. 1997

In five mechanically ventilated rabbits, we studied the property of inhaled nitric oxide in helping to treat hypoxaemia which was induced by intravenous endotoxin (Escherichia coli-derived lipopolysaccharide, serotype 0111: B4). We used measurements of arterial partial pressure of oxygen to check a therapeutic nitric oxide benefit. Pulmonary artery pressure was continuously monitored. Furthermore, we determined the single-breath diffusing capacity for nitric oxide. Measurements of plasma nitrite/nitrate concentration served as an indicator of endogenous nitric oxide output. The first infusion of endotoxin led to a transient pulmonary vasoconstriction, whereas arterial partial pressure of oxygen was permanently reduced by 30 +/- 10 mmHg (mean +/- SD), attaining minimal values of 48 +/- 3.4 mmHg due to additional endotoxin. Single-breath diffusing capacity for nitric oxide declined by 20 +/- 5.5% of baseline values until the experiments were concluded. Endotoxin induced an increase in plasma nitrite/nitrate concentration in the five rabbits as well as in the control animals (four rabbits) without exogenous nitric oxide supply. During the 25 inhalations of nitric oxide (3-50 ppm), arterial oxygenation did not change significantly. Thus endotoxin permanently impaired pulmonary gas exchange without inducing pulmonary hypertension. Inhaled nitric oxide did not improve arterial oxygenation during endotoxaemia.