Pulmonary Diffusing Capacity, Blood Flow and Tissue Volume by Rebreathing in Inhomogeneous Lung Models

Author(s):  
Michael Meyer ◽  
Christian Hook

1965 ◽  
Vol 20 (6) ◽  
pp. 1199-1204 ◽  
Author(s):  
Gordon G. Power ◽  
Richard W. Hyde ◽  
Raymond J. Sever ◽  
Frederic G. Hoppin ◽  
Jean R. Nairn

We studied possible causes of the decreased arterial oxygen saturation seen when a subject is accelerated in a centrifuge by measuring simultaneously the pulmonary diffusing capacity, DlCO, and the effective pulmonary capillary blood flow, Qc, using breath-holding techniques with carbon monoxide and acetylene. After 1 min of forward ("eyeballs in") acceleration at eight times normal gravity, 8 G, average Dl decreased 35% from an initial control of 33.7 to 21.5 ml/(min x mm Hg) in four subjects. Although this decrease was statistically significant, the values observed were not low enough to indicate that impaired diffusion was a prime cause of arterial unsaturation. Average Qc decreased 35% during acceleration from an initial control value of 12.9 to 8.2 liters/min, also a significant change. These values may have indicated that total pulmonary blood flow was reduced, but a more likely explanation is that a large portion of pulmonary flow perfused nonventilated regions. Dl and Qc returned toward initial control levels within 8 min after acceleration in most instances. lung volume during acceleration Submitted on March 1, 1965



1963 ◽  
Vol 18 (1) ◽  
pp. 123-128 ◽  
Author(s):  
Benjamin Burrows ◽  
Albert H. Niden

Hemorrhagic shock induced a marked fall in the pulmonary diffusing capacity for carbon monoxide in the dog (Dl) and produced marked nonuniformity of Dl/Va ratios throughout the lung as assessed by the “equilibration technique”. Difficulties in calculating over-all Dl under these conditions are discussed. Induced anemia also produced a fall in Dl, but little change in the uniformity of Dl/Va ratios was noted. In isolated perfused dog lungs where blood flow, pulmonary vascular pressures, lung volume, and ventilation were maintained constant, Dl was found to be proportional to hematocrit, suggesting either: 1) that virtually all resistance to CO diffusion is in the erythrocyte or 2) that the apparent diffusing capacity of the alveolar-capillary membrane is dependent upon hematocrit, carbon monoxide transfer being reduced across portions of membrane which are some distance from a red blood cell. Submitted on January 12, 1962



1982 ◽  
Vol 48 (2) ◽  
pp. 255-279 ◽  
Author(s):  
Christian Hook ◽  
Michael Meyer




1961 ◽  
Vol 16 (3) ◽  
pp. 499-506 ◽  
Author(s):  
Johannes Piiper ◽  
Pierre Haab ◽  
Hermann Rahn

In anesthetized dogs the alveolar-arterial O2 pressure difference (AaD) was measured at alveolar O2 pressures of 45, 75, 106, 146, and 255 mm Hg. The AaD values observed could not be explained by the conventional “shunt factor,” “diffusion-limitation factor,” or “distribution factor.” However, the experimental data could be explained on the basis of the concept of unequal distribution of pulmonary diffusing capacity, D, to perfusion, Q. A procedure for estimation of the pattern of distribution of D to Q from experimental data is described. The results were compatible with the assumption that the lung consisted of a minimum of three functional compartments characterized by different D/Q ratios. A small portion of the perfusion (1.5%) probably behaved like a true shunt (D/Q = 0); 13% of the pulmonary blood flow passed through a compartment that shared in 2% of the total diffusing capacity only, resulting in a relatively small D/Q ratio for this compartment. The presence of this compartment gave rise to the largest part of the AaD at air breathing. The calculated D/Q value for the remaining, major compartment was so high that a measurable AaD due to diffusion limitation in this compartment could occur only at alveolar O2 pressures lower than 60 mm Hg. The validity of the assumptions and the significance of the results are discussed. Submitted on May 23, 1960



1961 ◽  
Vol 16 (3) ◽  
pp. 493-498 ◽  
Author(s):  
Johannes Piiper

The effects of unequal distribution of pulmonary diffusing capacity to the pulmonary blood flow on the alveolar-arterial O2 pressure difference have been studied theoretically. It is demonstrated that, if the diffusing capacity is not distributed proportionally to the blood flow in a lung, the alveolar-arterial O2 pressure difference will in most circumstances be greater than in a lung with the same total diffusing capacity and the same total blood flow, but with equal distribution of diffusing capacity to blood flow. Submitted on May 23, 1960



1973 ◽  
Vol 52 (2) ◽  
pp. 359-369 ◽  
Author(s):  
Edward D. Michaelson ◽  
Marvin A. Sackner ◽  
Robert L. Johnson


2010 ◽  
Vol 109 (6) ◽  
pp. 1913-1919 ◽  
Author(s):  
Cuneyt Yilmaz ◽  
Priya Ravikumar ◽  
Dennis J. Bellotto ◽  
Roger H. Unger ◽  
Connie C. W. Hsia

The Zucker diabetic fatty (ZDF fa/fa) rat with genetic leptin insensitivity develops obesity and Type 2 diabetes mellitus (T2DM) with age accompanied by hyperplastic changes in the distal lung ( Am J Physiol Lung Cell Mol Physiol 298: L392–L403, 2010). To determine the functional consequences of structural changes, we developed a rebreathing (RB) technique to simultaneously measure lung volume, pulmonary blood flow, lung diffusing capacity (DlCO), membrane diffusing capacity (DmCO), pulmonary capillary blood volume (Vc), and septal tissue volume in anesthetized tracheostomized male ZDF fa/fa and matched lean (+/+) control animals at 4, 8, and 12 mo of age. Results obtained by RB technique were compared with that measured by a single-breath (SB) technique and to that expected in a wide range of species. In fa/fa animals compared with +/+, lung volumes and compliance were 13–35% lower at different ages, and the normal age-related increase in lung compliance was no longer evident. Mean pulmonary blood flow declined with age in fa/fa but not in +/+ animals. DlCO measured at a given pulmonary blood flow was 20–43% lower at different ages due to reductions in both DmCO and Vc. Septal tissue volume was also reduced in older fa/fa rats. We conclude that obese rats with T2DM develop significant restrictive pulmonary defects with diffusion impairment in a pattern similar to that previously reported in obese human subjects with T2DM. Functional impairment became exaggerated with age and duration of T2DM. In both fa/fa and +/+ animals, DlCO measured by RB was systematically higher than by SB technique whereas lung volume was similar, a finding consistent with heterogeneous distribution of ventilation in the rat lung.





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