scholarly journals High-altitude exposure of three weeks duration increases lung diffusing capacity in humans

2011 ◽  
Vol 110 (6) ◽  
pp. 1564-1571 ◽  
Author(s):  
Piergiuseppe Agostoni ◽  
Erik R. Swenson ◽  
Maurizio Bussotti ◽  
Miriam Revera ◽  
Paolo Meriggi ◽  
...  

Background: high-altitude adaptation leads to progressive increase in arterial PaO2. In addition to increased ventilation, better arterial oxygenation may reflect improvements in lung gas exchange. Previous investigations reveal alterations at the alveolar-capillary barrier indicative of decreased resistance to gas exchange with prolonged hypoxia adaptation, but how quickly this occurs is unknown. Carbon monoxide lung diffusing capacity and its major determinants, hemoglobin, alveolar volume, pulmonary capillary blood volume, and alveolar-capillary membrane diffusion, have never been examined with early high-altitude adaptation. Methods and Results: lung diffusion was measured in 33 healthy lowlanders at sea level (Milan, Italy) and at Mount Everest South Base Camp (5,400 m) after a 9-day trek and 2-wk residence at 5,400 m. Measurements were adjusted for hemoglobin and inspired oxygen. Subjects with mountain sickness were excluded. After 2 wk at 5,400 m, hemoglobin oxygen saturation increased from 77.2 ± 6.0 to 85.3 ± 3.6%. Compared with sea level, there were increases in hemoglobin, lung diffusing capacity, membrane diffusion, and alveolar volume from 14.2 ± 1.2 to 17.2 ± 1.8 g/dl ( P < 0.01), from 23.6 ± 4.4 to 25.1 ± 5.3 ml·min−1·mmHg−1 ( P < 0.0303), 63 ± 34 to 102 ± 65 ml·min−1·mmHg−1 ( P < 0.01), and 5.6 ± 1.0 to 6.3 ± 1.1 liters ( P < 0.01), respectively. Pulmonary capillary blood volume was unchanged. Membrane diffusion normalized for alveolar volume was 10.9 ± 5.2 at sea level rising to 16.0 ± 9.2 ml·min−1·mmHg−1·l−1 ( P < 0.01) at 5,400 m. Conclusions: at high altitude, lung diffusing capacity improves with acclimatization due to increases of hemoglobin, alveolar volume, and membrane diffusion. Reduction in alveolar-capillary barrier resistance is possibly mediated by an increase of sympathetic tone and can develop in 3 wk.

1965 ◽  
Vol 20 (1) ◽  
pp. 113-116 ◽  
Author(s):  
Denise Jouasset-Strieder ◽  
John M. Cahill ◽  
John J. Byrne ◽  
Edward A. Gaensler

The CO diffusing capacity (Dl) was measured by the single-breath method in eight anesthetized dogs. Pulmonary capillary blood volume (Vc) and membrane diffusing capacity (Dm) were determined in six animals by the method of Roughton and Forster. The studies were repeated after anemia had been induced by replacing whole blood with plasma. Large dogs were selected with a mean body weight of 29 kg and a mean alveolar volume of 2,020 ml (STPD) during tests. The mean arterial blood Hb decreased from 14.3 to 6.6 g/100 ml, the mean Dl from 27 to 12 ml/min mm Hg, and the mean Dm from 100 to 47 ml/min mm Hg. Vc averaged 67 ml in the control state and was not significantly changed during anemia. Reductions in Dl and Dm during anemia were proportional to the fall in blood Hb. Both Dl and Dm in all dogs, normal and anemic, were proportional to the volume of red blood cells in the lung capillaries (Vrbc). These results suggest that Vrbc might be an estimate of the useful area of the alveolar-capillary membrane while Dm/Vrbc should vary with changes in its thickness. The latter was not altered by anemia. alveolar capillary membrane; pulmonary membrane; diffusing capacity; pulmonary capillary RBC volume; pulmonary diffusion pathway; carbon monoxide Submitted on March 2, 1964


1960 ◽  
Vol 15 (5) ◽  
pp. 843-848 ◽  
Author(s):  
Joseph C. Ross ◽  
Thomas H. Lord ◽  
Glen D. Ley

Pressure-suit inflation over the lower body produces acute pulmonary hypertension. An increase in pulmonary capillary blood volume, Vc, with this procedure should theoretically increase pulmonary-diffusing capacity, Dl. Lewis and co-workers ( J. Appl. Physiol. 12:57, 1958) found no increase in Dl with suit inflation. The subject was reinvestigated with measurement of the increase in central venous pressure, CVP, produced and with a study of effect of alveolar volume, Va, and the Valsalva maneuver on the results. Dl was determined in five seated and seven supine subjects at small and large Va, both before and during suit inflation and also with a Valsalva under each condition. Suit inflation significantly increased Dl (13%) with an increase in 21 of the 22 comparisons. Mean Dl was 16% lower when Va was decreased 34%. The Valsalva maneuver significantly decreased both control and suit inflation Dl. Results show that with controlled Va and no Valsalva and when CVP was definitely increased by the procedure, Dl significantly increased with suit inflation, probably indicating that the pulmonary capillary bed was passively dilated. Submitted on March 11, 1960


2002 ◽  
Vol 93 (3) ◽  
pp. 931-935 ◽  
Author(s):  
Malin Rohdin ◽  
Dag Linnarsson

In normal gravity, lung diffusing capacity (Dl CO) and lung tissue volume (LTV; including pulmonary capillary blood volume) change in concert, for example, during shifts between upright and supine. Accordingly, Dl CO and LTV might be expected to decrease together in sitting subjects in hypergravity due to peripheral pooling of blood and reduced central blood volume. Nine sitting subjects in a human centrifuge were exposed to one, two, and three times increased gravity in the head-to-feet direction (Gz+) and rebreathed a gas containing trace amounts of acetylene and carbon monoxide. Dl CO was 25.2 ± 2.6, 20.0 ± 2.1, and 16.7 ± 1.7 ml · min−1 · mbar−1(means ± SE) at 1, 2, and 3 Gz+, respectively (ANOVA P < 0.001). Corresponding values for LTV increased from 541 ± 34 to 677 ± 43, and 756 ± 71 ml ( P < 0.001) at 2 and 3 Gz+. Results are compatible with sequestration of blood in the dependent part of the pulmonary circulation just as in the systemic counterpart. Dl CO, which under normoxic conditions is mainly determined by its membrane component, decreased despite an increased pulmonary capillary blood volume, most likely as a consequence of a less homogenous distribution of alveolar volume with respect to pulmonary capillary blood volume.


1997 ◽  
Vol 83 (3) ◽  
pp. 810-816 ◽  
Author(s):  
Sylvia Verbanck ◽  
Hans Larsson ◽  
Dag Linnarsson ◽  
G. Kim Prisk ◽  
John B. West ◽  
...  

Verbanck, Sylvia, Hans Larsson, Dag Linnarsson, G. Kim Prisk, John B. West, and Manuel Paiva. Pulmonary tissue volume, cardiac output and diffusing capacity in sustained microgravity. J. Appl. Physiol. 83(3): 810–816, 1997.—In microgravity (μG) humans have marked changes in body fluids, with a combination of an overall fluid loss and a redistribution of fluids in the cranial direction. We investigated whether interstitial pulmonary edema develops as a result of a headward fluid shift or whether pulmonary tissue fluid volume is reduced as a result of the overall loss of body fluid. We measured pulmonary tissue volume (Vti), capillary blood flow, and diffusing capacity in four subjects before, during, and after 10 days of exposure to μG during spaceflight. Measurements were made by rebreathing a gas mixture containing small amounts of acetylene, carbon monoxide, and argon. Measurements made early in flight in two subjects showed no change in Vti despite large increases in stroke volume (40%) and diffusing capacity (13%) consistent with increased pulmonary capillary blood volume. Late in-flight measurements in four subjects showed a 25% reduction in Vti compared with preflight controls ( P < 0.001). There was a concomittant reduction in stroke volume, to the extent that it was no longer significantly different from preflight control. Diffusing capacity remained elevated (11%; P< 0.05) late in flight. These findings suggest that, despite increased pulmonary perfusion and pulmonary capillary blood volume, interstitial pulmonary edema does not result from exposure to μG.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Egidio Beretta ◽  
Gabriele Simone Grasso ◽  
Greta Forcaia ◽  
Giulio Sancini ◽  
Giuseppe Miserocchi

Abstract Oxygen diffusion across the air-blood barrier in the lung is commensurate with metabolic needs and ideally allows full equilibration between alveolar and blood partial oxygen pressures. We estimated the alveolo-capillary O2 equilibration in 18 healthy subjects at sea level at rest and after exposure to increased O2 demand, including work at sea level and on hypobaric hypoxia exposure at 3840 m (PA ~ 50 mmHg). For each subject we estimated O2 diffusion capacity (DO2), pulmonary capillary blood volume (Vc) and cardiac output ($$\dot{Q}$$Q̇). We derived blood capillary transit time $${\boldsymbol{(}}{\boldsymbol{T}}{\boldsymbol{t}}{\boldsymbol{=}}\frac{{\boldsymbol{V}}{\boldsymbol{c}}}{\dot{{\boldsymbol{Q}}}}{\boldsymbol{)}}$$(Tt=VcQ̇) and the time constant of the equilibration process ($${\boldsymbol{\tau }}{\boldsymbol{=}}\frac{{\boldsymbol{\beta }}{\boldsymbol{V}}{\boldsymbol{c}}}{{\boldsymbol{D}}{{\boldsymbol{O}}}_{{\boldsymbol{2}}}}$$τ=βVcDO2, β being the slope of the hemoglobin dissociation curve). O2 equilibration at the arterial end of the pulmonary capillary was defined as $${{\bf{L}}}_{{\bf{e}}{\bf{q}}}{\boldsymbol{=}}{{\bf{e}}}^{{\boldsymbol{-}}\frac{{\bf{T}}t}{{\boldsymbol{\tau }}}}$$Leq=e−Ttτ. Leq greately differed among subjects in the most demanding O2 condition (work in hypoxia): lack of full equilibration was found to range from 5 to 42% of the alveolo-capillary PO2 gradient at the venous end. The present analysis proves to be sensible enough to highlight inter-individual differences in alveolo-capillary equilibration among healthy subjects.


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