On the Prediction of Pulmonary Diffusing Capacity with a Steady State Carbon Monoxide Method in Chronic Lung Diseases

1969 ◽  
Vol 24 (4) ◽  
pp. 377-381
Author(s):  
S. Gabriel
1963 ◽  
Vol 18 (3) ◽  
pp. 447-456 ◽  
Author(s):  
G. M. Turino ◽  
E. H. Bergofsky ◽  
R. M. Goldring ◽  
A. P. Fishman

The effect of graded exercise on the pulmonary diffusing capacity for both oxygen and carbon monoxide measured simultaneously was studied in healthy young adults by steady-state methods. Pulmonary diffusing capacity for oxygen increases progressively with increasing severity of exercise; it exceeds the DlCO at high levels of exercise by amounts greater than can be accounted for by the difference in diffusivity of the test gases. Diffusing capacity for carbon monoxide increases less than DlOO2 for comparable grades of exercise but no definite plateau value could be established. The supine or upright body position does not influence the values of either DlOO2 or DlCO during exercise. Diffusing capacity of the lung for oxygen does not limit the maximum levels of exercise which may be achieved by normal man. Submitted on August 6, 1962


1957 ◽  
Vol 188 (2) ◽  
pp. 355-359 ◽  
Author(s):  
A. B. Otis ◽  
James Jude

Measurements were made of the arterial-alveolar carbon dioxide gradient in anesthetized dogs at body temperatures ranging from normal down to 16°C. Pulmonary diffusing capacity was determined by a steady-state carbon monoxide method in anesthetized dogs at normal body temperatures and at 25°C. From the results it is concluded that although diffusing capacity is reduced at low body temperatures, it is still adequate for transfer of both CO2 and O2 because the metabolic requirements for gas exchange are also reduced.


Thorax ◽  
1959 ◽  
Vol 14 (2) ◽  
pp. 166-175 ◽  
Author(s):  
J. MacNamara ◽  
F. J. Prime ◽  
J. D. Sinclair

1963 ◽  
Vol 18 (1) ◽  
pp. 89-96 ◽  
Author(s):  
Kaye H. Kilburn ◽  
Harry A. Miller ◽  
John E. Burton ◽  
Ronald Rhodes

Alterations in the steady-state diffusing capacity for carbon monoxide (Dco) by the method of Filley, MacIntosh, and Wright, produced by sequential changes in the pattern of breathing were studied in anesthetized, paralyzed, artificially ventilated dogs. The Dco of paralyzed, artificially ventilated control dogs did not differ significantly during 3 hr from values found in conscious and anesthetized controls. A fivefold increase in tidal volume without changing frequency of breathing raised alveolar ventilation and CO uptake 500% and Dco 186%. A high correlation between tidal volume and Dco was noted during reciprocal alterations of tidal volume and rate which maintained minute volume. The Dco appeared to fall when alveolar ventilation was tripled by increments of rate with a fixed-tidal volume, despite a 63% increase in CO uptake. Doubling end-expiratory lung volume by positive pressure breathing without altering tidal volume or rate did not affect Dco. The addition of 100 ml of external dead space with rate and tidal volume constant decreased Dco to 42% of control level, however, stepwise reduction of dead space from 100 ml to 0 in two dogs failed to change Dco. Added dead space equal to frac12 tidal volume (170 ml) reduced Dco to 25% of control in two dogs with a return to control with removal of dead space. Thus, in paralyzed artificially ventilated dogs, tidal volume appears to be the principal ventilatory determinant of steady-state Dco. Dco is minimally affected by increases in alveolar ventilation with a constant tidal volume effected by increasing the frequency of breathing. Prolonged ventilation, at fixed rate and volume, and increased dead space either did not effect, or they reduced Dco, perhaps by rendering less uniform the distribution of gas, and blood in the lungs. Although lung volume was doubled by positive-pressure breathing, pulmonary capillary blood volume was probably reduced to produce opposing effects on diffusing capacity and no net change. Submitted on March 14, 1962


1981 ◽  
Vol 50 (5) ◽  
pp. 1061-1064 ◽  
Author(s):  
D. Z. Rubin ◽  
D. Fujino ◽  
C. Mittman ◽  
S. M. Lewis

The existence of a saturable carbon monoxide (CO) carrier in the lung remains controversial. The carrier hypothesis was invoked to explain data that indicated that pulmonary diffusing capacity for CO (DLCO) decreases with increasing CO concentration. To test this hypothesis, we measured DLCO in 14 normal adult subjects at three alveolar CO concentrations (60, 660, and 2,060 ppm). Each mixture contained a constant amount of labeled C18O (60 ppm) and a balance of unlabeled C16O. If a saturable carrier exists at increasing CO concentrations, the unlabeled CO would compete for most of the sites on the carrier molecule, effectively inhibiting the uptake of the labeled C18O. C18O diffusing capacities (mean +/- SD) for the three levels of CO were 34.9 +/- 5.6, 33.0 +/- 6.0, and 34.7 +/- 7.8. There were no significant differences (P greater than 0.2) among the three levels. In another group of subjects we repeated the study using a gas mixture containing 130 ppm C18O. No significant differences were found. As a result, we find no evidence to support a CO carrier hypothesis.


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