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1

Boselli, E., and B. Allaouchiche. "Diffusion pulmonaire des antibiotiques.Analyse critique de la littérature." Annales Françaises d'Anesthésie et de Réanimation 20, no. 7 (2001): 612–30. http://dx.doi.org/10.1016/s0750-7658(01)00439-7.

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2

Rouatbi, S., Y. F. Ouahchi, C. Ben Salah, et al. "Facteurs physiologiques influençant le volume capillaire pulmonaire et la diffusion membranaire." Revue des Maladies Respiratoires 23, no. 3 (2006): 211–18. http://dx.doi.org/10.1016/s0761-8425(06)71570-4.

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3

Boselli, E. "Diffusion pulmonaire des céphalosporines de troisième génération : perfusion continue versus administration intermittente." Antibiotiques 7, no. 2 (2005): 117–23. http://dx.doi.org/10.1016/s1294-5501(05)80177-3.

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4

Boussana, A., O. Hue, M. Hayot, S. Matécki, M. Ramonatxo, and D. Le Gallais. "Capacité de diffusion pulmonaire avant un triathlon et 24 heures après la compétition." Science & Sports 15, no. 5 (2000): 245–47. http://dx.doi.org/10.1016/s0765-1597(00)80035-0.

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5

Sivova, N., D. Launay, G. Denis, et al. "Évaluation de l’atteinte pulmonaire de la sclérodermie systémique par la méthode de double diffusion DLCO/DLNO." La Revue de Médecine Interne 32 (December 2011): S307—S308. http://dx.doi.org/10.1016/j.revmed.2011.10.389.

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6

Stern, J. B., Y. Péan, P. Girard, et al. "Empyème après chirurgie d’exérèse pulmonaire : étude de la diffusion pleurale de l’amoxicilline et de la vancomycine." Revue des Maladies Respiratoires 24, no. 7 (2007): 853–58. http://dx.doi.org/10.1016/s0761-8425(07)91387-x.

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7

Mribah, H., M. Hafsa, I. Touil, et al. "La valeur pronostique de la diffusion du monoxyde de carbone au cours de la fibrose pulmonaire idiopathique." Revue des Maladies Respiratoires 34 (January 2017): A127. http://dx.doi.org/10.1016/j.rmr.2016.10.298.

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8

Stern, J. B., P. Girard, Y. Péan, et al. "328 Empyème après chirurgie d’exérèse pulmonaire majeure : étude de la diffusion pleurale de l’amoxicilline et de la vancomycine." Revue des Maladies Respiratoires 24 (January 2007): 104. http://dx.doi.org/10.1016/s0761-8425(07)72704-3.

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9

Bados, A. "Détermination du volume capillaire pulmonaire par méthode en double diffusion NO-CO chez les enfants drépanocytaires. Étude pilote." Revue des Maladies Respiratoires 24, no. 1 (2007): 88. http://dx.doi.org/10.1016/s0761-8425(07)91019-0.

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10

Masse, G., M. L. Choukroun, M. Fayon, et al. "SFP-P158 – Hépatologie, gastro-entérologie et nutrition – Diffusion membranaire et volume capillaire pulmonaire dans la maladie de Crohn." Archives de Pédiatrie 15, no. 5 (2008): 990–91. http://dx.doi.org/10.1016/s0929-693x(08)72288-7.

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11

Perez, T., G. Denis, N. Bautin, et al. "512 Intérêt du volume capillaire pulmonaire par la technique de la double diffusion CO-NO dans la sclérodermie systémique." Revue des Maladies Respiratoires 24 (January 2007): 154. http://dx.doi.org/10.1016/s0761-8425(07)72889-9.

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12

Couraud, S., C. Fontaine-Delaruelle, A. Hassouni, et al. "Évolution de la double diffusion au CO et au NO au cours de la radiothérapie pulmonaire pour cancer bronchique : l’étude prospective CONORT." Revue des Maladies Respiratoires 32 (January 2015): A123. http://dx.doi.org/10.1016/j.rmr.2014.10.641.

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13

Tiev, K. P., N. N. Ledong, S. Riviere, et al. "Prédiction de la survenue de l’hypertension pulmonaire au cours de la sclérodermie systémique par le coefficient de diffusion de la membrane alvéolaire." La Revue de Médecine Interne 32 (June 2011): S96. http://dx.doi.org/10.1016/j.revmed.2011.03.122.

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14

Perrin, F., A. Chambellan, E. Mourrain-Langlois, et al. "Étude des mesures du volume capillaire et du facteur membranaire par double diffusion pulmonaire CO/NO chez 73 patients suivis pour une sclérodermie systémique." La Revue de Médecine Interne 32 (June 2011): S98. http://dx.doi.org/10.1016/j.revmed.2011.03.125.

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15

Zarza, V., S. Couraud, A. Hassouni, et al. "Évolution de la double diffusion au CO et au NO au cours de la radiothérapie pulmonaire pour cancer bronchique : présentation du protocole de l’étude prospective Conort." Cancer/Radiothérapie 18, no. 5-6 (2014): 420–24. http://dx.doi.org/10.1016/j.canrad.2014.07.152.

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16

Rosyid, Alfian Nur, and Isnin Anang Marhana. "Faal Paru Difusi." Jurnal Respirasi 4, no. 2 (2018): 61. http://dx.doi.org/10.20473/jr.v4-i.2.2018.61-70.

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Diffusion capacity is useful for measuring ability of pulmonary microcirculation to transfer oxygen and carbon dioxide from alveoli to capillaries. Physiological examination of diffusion is a continuation of physiological examination of ventilation. Diffusion capacity is measured by DLCO (Diffusing capacity for Carbon Monoxide). Measurement of oxygen diffusion capacity directly is very difficult so that indirect methods are used using carbonmonoxide (DLCO). Diffusion capacity of oxygen is equivalent to DLCO multiplied by 1.23. Normal value of DLCO is 20-30 ml/minute mmHg. Some factors that affect DLCO are Hb levels, COHb in smokers, and alveolar volume. Some techniques for measuring DLCO include Steady-state, Three-equation Single-breath, Nitrogen Washout, and Intra-breath DLCO. This test is indicated in pulmonary parenchymal disease (pulmonary fibrosis, asbestosis, sarcoidosis, interstitial lung disease), cystic fibrosis, pulmonary hypertension, and pulmonary bleeding. DLCO is increased in asthma patients, obesity, polycythemia, intraalveolar bleeding, and right-left heart shunting. DLCO is decreased in emphysematous lung patients, pulmonary post resection, bronchial obstruction, multiple pulmonary embolism, anemia, idiopathic pulmonary fibrosis, asbestosis, sarcoidosis, vascular collagen disease, hypersensitive pneumonitis, and alveolar proteinosis.
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17

Allanore, Y., D. Borderie, J. Avouac, et al. "Une augmentation du NTproBNP et une diminution de la diffusion du monoxyde de carbone sont des facteurs prédictifs indépendants d'hypertension artérielle pulmonaire au cours de la sclérodermie systémique." Revue du Rhumatisme 74, no. 10-11 (2007): 1185. http://dx.doi.org/10.1016/j.rhum.2007.10.382.

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18

Frank, Andreas O., C. J. Charles Chuong, and Robert L. Johnson. "A finite-element model of oxygen diffusion in the pulmonary capillaries." Journal of Applied Physiology 82, no. 6 (1997): 2036–44. http://dx.doi.org/10.1152/jappl.1997.82.6.2036.

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Frank, Andreas O., C. J. Charles Chuong, and Robert L. Johnson. A finite-element model of oxygen diffusion in the pulmonary capillaries. J. Appl. Physiol. 82(6): 2036–2044, 1997.—We determined the overall pulmonary diffusing capacity (Dl) and the diffusing capacities of the alveolar membrane (Dm) and the red blood cell (RBC) segments (De) of the diffusional pathway for O2 by using a two-dimensional finite-element model developed to represent the sheet-flow characteristics of pulmonary capillaries. An axisymmetric model was also considered to assess the effect of geometric configuration. Results showed the membrane segment contributing the major resistance, with the RBC segment resistance increasing as O2 saturation ([Formula: see text]) rises during the RBC transit: RBC contributed 7% of the total resistance at the capillary inlet ([Formula: see text] = 75%) and 30% toward the capillary end ([Formula: see text] = 95%) for a 45% hematocrit (Hct). Both Dm and Dlincreased as the Hct increased but began approaching a plateau near an Hct of 35%, due to competition between RBCs for O2 influx. Both Dm and Dl were found to be relatively insensitive (2∼4%) to changes in plasma protein concentration (28∼45%). Axisymmetric results showed similar trends for all Hct and protein concentrations but consistently overestimated the diffusing capacities (∼2.2 times), primarily because of an exaggerated air-tissue barrier surface area. The two-dimensional model correlated reasonably well with experimental data and can better represent the O2 uptake of the pulmonary capillary bed.
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19

Agostoni, Piergiuseppe, Erik R. Swenson, Maurizio Bussotti, et al. "High-altitude exposure of three weeks duration increases lung diffusing capacity in humans." Journal of Applied Physiology 110, no. 6 (2011): 1564–71. http://dx.doi.org/10.1152/japplphysiol.01167.2010.

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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.
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20

Hsia, C. C., C. J. Chuong, and R. L. Johnson. "Critique of conceptual basis of diffusing capacity estimates: a finite element analysis." Journal of Applied Physiology 79, no. 3 (1995): 1039–47. http://dx.doi.org/10.1152/jappl.1995.79.3.1039.

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We present a simple geometric model of a pulmonary capillary segment containing a variable number of red blood cells. The pattern of CO transfer from alveolar air to capillary red blood cells in this model is accurately computed by a finite element method and used to explore conceptual flaws in the Roughton-Forster (RF) and morphometric methods of estimating pulmonary diffusing capacity for CO. The CO uptakes calculated by the finite element method at two alveolar O2 tensions are introduced into the RF model to determine whether the anatomically defined membrane component of diffusing capacity for CO (DmCO) and pulmonary capillary blood volume (Vc) are recovered. The same capillary model is also subjected to standard morphometric analysis. Results are compared at different levels of capillary hematocrit (Hct). The RF method accurately recovers DmCO and Vc at a low Hct but modestly overestimates DmCO and underestimates Vc at higher Hct; errors arise because conductance of the tissue-plasma membrane for CO varies with alveolar O2 tension. The morphometric method seriously overestimates DmCO because the true tissue-plasma resistance to diffusion is underestimated and the effective membrane utilized for diffusion is overestimated; these errors are accentuated by a low Hct.
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21

Heming, T. A., E. K. Stabenau, C. G. Vanoye, H. Moghadasi, and A. Bidani. "Roles of intra- and extracellular carbonic anhydrase in alveolar-capillary CO2 equilibration." Journal of Applied Physiology 77, no. 2 (1994): 697–705. http://dx.doi.org/10.1152/jappl.1994.77.2.697.

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Alveolar-capillary CO2 equilibration involves diffusive equilibration of CO2 across the blood-gas barrier and chemical equilibration of perfusate CO2-HCO-3-H+ reactions. These processes are governed by different, but related, driving forces and conductances. The present study examined the importance of pulmonary carbonic anhydrase (CA) for diffusive and reactive CO2 equilibration in isolated rat lungs. Lungs were perfused with salines containing membrane-impermeant or -permeant inhibitors of CA. Measurements of CO2 excretion rate, equilibrated venous and arterial PCO2 and pH, and postcapillary pH and PCO2 disequilibria were used, together with our previous model of CO2-HCO-3-H+ reactions and transport in saline-perfused capillaries (Bidani et al. J. Appl. Physiol. 55: 75–83, 1983), to compute the relevant driving forces and conductances. Reactive CO2 equilibration was markedly affected by extracellular (vascular) CA activity but not by the activity of intracellular (cytosolic) CA. The driving force for CO2 diffusion was strongly influenced by vascular CA activity. The conductance for CO2 diffusion was independent of CA activity. The minimum conductance for CO2 diffusion was estimated to be 700–800 ml.min-1.Torr-1. The results indicate that extracellular vascular CA activity influences both diffusive and reactive CO2 equilibration. However, cytosolic CA has no detectable role in alveolar-capillary CO2 equilibration.
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22

Kanick, Stephen Chad, William J. Doyle, Samir N. Ghadiali, and William J. Federspiel. "On morphometric measurement of oxygen diffusing capacity in middle ear gas exchange." Journal of Applied Physiology 98, no. 1 (2005): 114–19. http://dx.doi.org/10.1152/japplphysiol.00203.2004.

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An accurate mathematical model of transmucosal gas exchange is prerequisite to understanding middle ear (ME) physiology. Current models require experimentally measured gas species time constants for all extant conditions as input parameters. However, studies on pulmonary gas exchange have shown that a morphometric model that incorporates more fundamental physiochemical and anatomic parameters accurately simulates transport from which the species time constants can be derived for all extant conditions. Here, we implemented a variant of that model for ME gas exchange that requires the measurement of diffusional length (τ) for the ME mucosa. That measure contributes to the mucosal diffusing capacity and reflects the resistance to gas flow between air space and capillary. Two methods for measuring τ have been proposed: linear distance between the air-mucosal boundary and capillary and the harmonic mean of all contributing pathway lengths. Oxygen diffusing capacity was calculated for different ME mucosal geometries by using the two τ measures, and the results were compared with those predicted by a detailed, two-dimensional finite element analysis. Predictive accuracy was improved by incorporating the harmonic τ measure, which captures important information regarding variations in capillary shape and distribution. However, compared with the oxygen diffusing capacity derived from the finite element analysis, both measures yielded nonlinear, positively biased estimates. The morphometric techniques underestimate diffusion length by failing to account for the curvilinear gas flow pathways predicted by the finite element model.
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23

Nabors, L. Karina, William A. Baumgartner, Steven J. Janke, James R. Rose, Wiltz W. Wagner, and Ronald L. Capen. "Red blood cell orientation in pulmonary capillaries and its effect on gas diffusion." Journal of Applied Physiology 94, no. 4 (2003): 1634–40. http://dx.doi.org/10.1152/japplphysiol.01021.2001.

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When alveoli are inflated, the stretched alveolar walls draw their capillaries into oval cross sections. This causes the disk-shaped red blood cells to be oriented near alveolar gas, thereby minimizing diffusion distance. We tested these ideas by measuring red blood cell orientation in histological slides from rapidly frozen rat lungs. High lung inflation did cause the capillaries to have oval cross sections, which constrained the red blood cells within them to flow with their broad sides facing alveolar gas. Low lung inflation stretched alveolar walls less and allowed the capillaries to assume a circular cross section. The circular luminal profile permitted the red blood cells to have their edges facing alveolar gas, which increased the diffusion distance. Using a finite-element method to calculate the diffusing capacity of red blood cells in the broad-side and edge-on orientations, we found that edge-on red blood cells had a 40% lower diffusing capacity. This suggests that, when capillary cross sections become circular, whether through low-alveolar volume or through increased microvascular pressure, the red blood cells are likely to be less favorably oriented for gas exchange.
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24

Dane, D. Merrill, Connie C. W. Hsia, Eugene Y. Wu, et al. "Splenectomy impairs diffusive oxygen transport in the lung of dogs." Journal of Applied Physiology 101, no. 1 (2006): 289–97. http://dx.doi.org/10.1152/japplphysiol.01600.2005.

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The spleen acts as an erythrocyte reservoir in highly aerobic species such as the dog and horse. Sympathetic-mediated splenic contraction during exercise reversibly enhances convective O2 transport by increasing hematocrit, blood volume, and O2-carrying capacity. Based on theoretical interactions between erythrocytes and capillary membrane (Hsia CCW, Johnson RL Jr, and Shah D. J Appl Physiol 86: 1460–1467, 1999) and experimental findings in horses of a postsplenectomy reduction in peripheral O2-diffusing capacity (Wagner PD, Erickson BK, Kubo K, Hiraga A, Kai M, Yamaya Y, Richardson R, and Seaman J. Equine Vet J 18, Suppl: 82–89, 1995), we hypothesized that splenic contraction also augments diffusive O2 transport in the lung. Therefore, we have measured lung diffusing capacity (DlCO) and its components during exercise by a rebreathing technique in six adult foxhounds before and after splenectomy. Splenectomy eliminated exercise-induced polycythemia, associated with a 30% reduction in maximal O2 uptake. At any given pulmonary blood flow, DlCO was significantly lower after splenectomy owing to a lower membrane diffusing capacity, whereas pulmonary capillary blood volume changed variably; microvascular recruitment, indicated by the slope of the increase in DlCO with respect to pulmonary blood flow, was also reduced. We conclude that splenic contraction enhances both convective and diffusive O2 transport and provides another compensatory mechanism for maintaining alveolar O2 transport in the presence of restrictive lung disease or ambient hypoxia.
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25

Hsia, Connie C. W., Robert L. Johnson, and Dipen Shah. "Red cell distribution and the recruitment of pulmonary diffusing capacity." Journal of Applied Physiology 86, no. 5 (1999): 1460–67. http://dx.doi.org/10.1152/jappl.1999.86.5.1460.

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The distribution of red blood cells in alveolar capillaries is typically nonuniform, as shown by intravital microscopy and in alveolar tissue fixed in situ. To determine the effects of red cell distribution on pulmonary diffusive gas transport, we computed the uptake of CO across a two-dimensional geometric capillary model containing a variable number of red blood cells. Red blood cells are spaced uniformly, randomly, or clustered without overlap within the capillary. Total CO diffusing capacity (Dl CO) and membrane diffusing capacity (DmCO) are calculated by a finite-element method. Results show that distribution of red blood cells at a fixed hematocrit greatly affects capillary CO uptake. At any given average capillary red cell density, the uniform distribution of red blood cells yields the highest DmCO and Dl CO, whereas the clustered distribution yields the lowest values. Random nonuniform distribution of red blood cells within a single capillary segment reduces diffusive CO uptake by up to 30%. Nonuniform distribution of red blood cells among separate capillary segments can reduce diffusive CO uptake by >50%. This analysis demonstrates that pulmonary microvascular recruitment for gas exchange does not depend solely on the number of patent capillaries or the hematocrit; simple redistribution of red blood cells within capillaries can potentially account for 50% of the observed physiological recruitment of Dl CO from rest to exercise.
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26

Gumbiene, Lina, Lina Kapleriene, Dovile Jancauskaite, et al. "Insights to correlations and discrepancies between impaired lung function and heart failure in Eisenmenger patients." Pulmonary Circulation 10, no. 1 (2020): 135065012090972. http://dx.doi.org/10.1177/2045894019899239.

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Impaired lung function and spirometric signs of airway obstruction without common risk factors for chronic obstructive pulmonary disease could be found in patients with Eisenmenger syndrome. This study aimed to analyse the association between lung function parameters and disease severity (including heart failure markers, associated congenital heart defect) as well as the possible reasons for airflow obstruction in Eisenmenger syndrome. The data of 25 patients with Eisenmenger syndrome were retrospectively evaluated. The patients were divided into groups according to airflow obstruction and a type of congenital heart defect. Airflow obstruction was found in nearly third (32%) of our cases and was associated with older age and worse survival. No relation was found between airway obstruction, B-type natriuretic peptide level, complexity of congenital heart defect and bronchial compression. Most of the patients (88%) had gas diffusion abnormalities. A weak negative correlation was noticed between gas diffusion (diffusing capacity of the lung for carbon monoxide) and B-type natriuretic peptide level (r = −0.437, p = 0.033). Increased residual volume was associated with higher mortality (p = 0.047 and p = 0.021, respectively). A link between B-type natriuretic peptide and lung diffusion, but not airway obstruction, was found. Further research and larger multicentre studies are needed to evaluate the importance of pulmonary function parameters and mechanisms of airflow obstruction in Eisenmenger syndrome.
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27

Kahraman, Adem, Mustafa Kahraman, Erol Bozdoğan, Fatih Alper, and Metin Akgün. "Toraks difüzyon manyetik rezonans görüntüleme." Tuberk Toraks 62, no. 3 (2014): 215–30. http://dx.doi.org/10.5578/tt.8317.

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28

Hsia, C. C. W., J. I. Carlin, M. Ramanathan, S. S. Cassidy, and R. L. Johnson. "Estimation of diffusion limitation after pneumonectomy from carbon monoxide diffusing capacity." Respiration Physiology 83, no. 1 (1991): 11–21. http://dx.doi.org/10.1016/0034-5687(91)90089-2.

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29

GUAZZI, Marco, and Piergiuseppe AGOSTONI. "Angiotensin-converting enzyme inhibition restores the diffusing capacity for carbon monoxide in patients with chronic heart failure by improving the molecular diffusion across the alveolar capillary membrane." Clinical Science 96, no. 1 (1999): 17–22. http://dx.doi.org/10.1042/cs0960017.

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Conductance of alveolar capillary membrane (DM) and capillary blood volume (VC) are the subcomponents of the pulmonary diffusing capacity for carbon monoxide (DLco). In chronic heart failure, stress failure of the membrane provides a mechanism for reduced DM and subsequent impairment of DLco. Angiotensin-converting enzyme inhibition improves DLco in patients with chronic heart failure. This study was aimed at investigating which of the two subcomponents of DLco is affected by angiotensin-converting enzyme inhibitors. Twenty-seven patients with NYHA class II to III chronic heart failure (group 1) and 13 age- and sex-matched normal subjects underwent pulmonary function testing with determination of DM and VC, while receiving placebo and 48 ;h and 1 and 2 months after starting enalapril treatment (10 ;mg twice daily). Nine similar patients (group 2) received isosorbide dinitrate (40 ;mg thrice daily) for a month then enalapril for another month, and underwent pulmonary function testing at 48 ;h and 1 month after starting treatments. Effects of angiotensin-converting enzyme inhibition in normal controls were not significant in the short- or mid-term. In group 1 patients, the only change observed at 48 ;h was a reduction in VC (probably due to a decrease in capillary pulmonary pressure). There was a marked increase in DM to a similar extent at 1 and 2 months, resulting in a significant improvement in DLco despite a decrease in VC. In group 2 patients, nitrates failed to improve DLco and DM, whereas enalapril was as effective as in group 1. These observations suggest a modulatory effect of angiotensin-converting enzyme inhibition on the membrane function which emerges gradually and persists over time and is probably dissociated from changes in pulmonary capillary pressure and VC. Chronic heart failure disturbs the alveolar capillary interface and increases gas diffusion resistance; angiotensin-converting enzyme inhibition restores the diffusive properties of the membrane and gas transfer, and protects the lung when the heart is failing.
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30

Leonova, E. I., E. I. Shmelev, and R. B. Amansakhedov. "Intracardiac hemodynamic abnormalities in patients with sarcoidosis." Russian Pulmonology 28, no. 5 (2018): 567–75. http://dx.doi.org/10.18093/0869-0189-2018-28-5-567-575.

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The aim of this study was to evaluate intracardiac hemodynamic abnormalities in patients with pulmonary sarcoidosis and to investigate relevant factors. Methods. The study involved 42 patients with chronic pulmonary sarcoidosis. Chest computed tomography (CT), echocardiography, body plethysmography, spirometry, 6-minute walking test, and measurements of lung diffusing capacity (DLCO), blood gases and blood C-reactive protein (CRP) were performed in all patients. Results. Chronic cor pulmonale was detected in 26.2% of patients. The right heart diastolic dysfunction was found in 14.3% of patients, the left heart diastolic dysfunction was found in 23.8% of patients, the mean pulmonary artery pressure (mPAP) was increased in 19% of patients. The right ventricular diameter was found to be related to the inspiratory bronchial resistance (Rin) (R = 0.480; p = 0.02), the intrathoracic gas volume (ITGV) (R = –0.670; p = 0.001), DLCO (R = 0.438; p = 0.013), and pulmonary fibrosis. The right heart systolic function (TAPSE) was related to DLCO (R = 0.518; p = 0.006), the total lung capacity (TLC) (R = 0.639; p = 0.001) and pulmonary fibrosis. The increased mPAP was related to the extension of disseminated lung lesions (R = 0.716; p = 0.018), blood oxygen partial pressure (R = 0.486; p = 0.017) and CRP level. The 6-min distance was related to Rin, the right ventricular diameter, parameters of the right heart diastolic function (tricuspid E / A ratio) (R = 0.486; p = 0.01), and ITGV (R = 0.494; p = 0.006). Conclusion. The development of cor pulmonale in patients with pulmonary sarcoidosis was related to DLCO, Rin and pulmonary fibrosis. The extension of disseminated lung lesions, hypoxemia and increased CRP were related to pulmonary hypertension. Different factors associated with cor pulmonale and pulmonary hypertension in sarcoidosis could prompt further investigation of different phenotypes of this disease with the intrinsic central hemodynamic abnormalities.
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31

Savushkina, O. I., A. V. Cherniak, E. V. Kryukov, et al. "Pulmonary function after COVID-19 in early convalescence phase." Medical alphabet, no. 25 (October 26, 2020): 7–12. http://dx.doi.org/10.33667/2078-5631-2020-25-7-12.

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Pulmonary function after COVID-19 in early convalescence phase. The aim of the study is to investigate the influence of Coronavirus disease 2019 (COVID-19) on pulmonary function in early convalescence phase.Materials and methods. The study included 44 patients (35 male) after COVID-19 without concomitant bronchopulmonary pathology, with a median age of 47.5 years. All patients underwent standard pulmonary function tests (PFTs): spirometry, body plethysmography, diffusion test. Besides, dyspnea on the mMRC scale was assessed, oxygen saturation level (SpO2 ) was measured. Depending on degree of lung damage determined using high-resolution computed tomography (CT), the patients were divided into 2 groups: group 1 (22 patients) — CT 1 and CT 2, group 2 (22 patients) — CT 3 and CT 4.Results. The medians of standard PFTs parameters were in normal values. However, there were statistically significant differences between groups: VC, FVC, FEV1 and TLC were lower in second group. Diffusing capacity was reduced in 52% of patients. Statistical significant correlations were established between lung damage by CT and the parameters of VC, FVC, FEV1 , TLC, IC and DLCO.Conclusion. The degree of functional disorders of lungs depended on the extent of abnormal CT. Impaired diffusing capacity were detected in more than half of the COVID-19 patients in early convalescence phase.
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Hsia, Connie C. W., Robert L. Johnson, D. Merrill Dane, et al. "The canine spleen in oxygen transport: gas exchange and hemodynamic responses to splenectomy." Journal of Applied Physiology 103, no. 5 (2007): 1496–505. http://dx.doi.org/10.1152/japplphysiol.00281.2007.

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In athletic animals the spleen induces acute polycythemia by dynamic contraction that releases red blood cells into the circulation in response to increased O2 demand and metabolic stress; when energy demand is relieved, the polycythemia is rapidly reversed by splenic relaxation. We have shown in adult foxhounds that splenectomy eliminates exercise-induced polycythemia, thereby reducing peak O2 uptake and lung diffusing capacity for carbon monoxide (DLCO) as well as exaggerating preexisting DLCO impairment imposed by pneumonectomy (Dane DM, Hsia CC, Wu EY, Hogg RT, Hogg DC, Estrera AS, Johnson RL Jr. J Appl Physiol 101: 289–297, 2006). To examine whether the postsplenectomy reduction in DLCO leads to abnormalities in O2 diffusion, ventilation-perfusion inequality, or hemodynamic function, we studied these animals via the multiple inert gas elimination technique at rest and during exercise at a constant workload equivalent to 50% or 80% of peak O2 uptake while breathing 21% and 14% O2 in balanced order. From rest to exercise after splenectomy, minute ventilation was significantly elevated with respect to O2 uptake compared with exercise before splenectomy; cardiac output, O2 delivery, and mean pulmonary and systemic arterial blood pressures were 10–20% lower, while O2 extraction was elevated with respect to O2 uptake. Ventilation-perfusion inequality was unchanged, but O2 diffusing capacities of lung (DLO2) and peripheral tissue during exercise were lower with respect to cardiac output postsplenectomy by 32% and 25%, respectively. The relationship between DLO2 and DLCO was unchanged by splenectomy. We conclude that the canine spleen regulates both convective and diffusive O2 transport during exercise to increase maximal O2 uptake.
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Kaushik, S. Sivaram, Matthew S. Freeman, Suk W. Yoon, et al. "Measuring diffusion limitation with a perfusion-limited gas—Hyperpolarized 129Xe gas-transfer spectroscopy in patients with idiopathic pulmonary fibrosis." Journal of Applied Physiology 117, no. 6 (2014): 577–85. http://dx.doi.org/10.1152/japplphysiol.00326.2014.

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Although xenon is classically taught to be a “perfusion-limited” gas, 129Xe in its hyperpolarized (HP) form, when detected by magnetic resonance (MR), can probe diffusion limitation. Inhaled HP 129Xe diffuses across the pulmonary blood-gas barrier, and, depending on its tissue environment, shifts its resonant frequency relative to the gas-phase reference (0 ppm) by 198 ppm in tissue/plasma barrier and 217 ppm in red blood cells (RBCs). In this work, we hypothesized that in patients with idiopathic pulmonary fibrosis (IPF), the ratio of 129Xe spectroscopic signal in the RBCs vs. barrier would diminish as diffusion-limitation delayed replenishment of 129Xe magnetization in RBCs. To test this hypothesis, 129Xe spectra were acquired in 6 IPF subjects as well as 11 healthy volunteers to establish a normal range. The RBC:barrier ratio was 0.55 ± 0.13 in healthy volunteers but was 3.3-fold lower in IPF subjects (0.16 ± 0.03, P = 0.0002). This was caused by a 52% reduction in the RBC signal ( P = 0.02) and a 58% increase in the barrier signal ( P = 0.01). Furthermore, the RBC:barrier ratio strongly correlated with lung diffusing capacity for carbon monoxide (DLCO) ( r = 0.89, P < 0.0001). It exhibited a moderate interscan variability (8.25%), and in healthy volunteers it decreased with greater lung inflation ( r = −0.78, P = 0.005). This spectroscopic technique provides a noninvasive, global probe of diffusion limitation and gas-transfer impairment and forms the basis for developing 3D MR imaging of gas exchange.
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Wu, E. Y., M. Ramanathan, and C. C. Hsia. "Role of hematocrit in the recruitment of pulmonary diffusing capacity: comparison of human and dog." Journal of Applied Physiology 80, no. 3 (1996): 1014–20. http://dx.doi.org/10.1152/jappl.1996.80.3.1014.

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In dogs, maximal O2 uptake (VO2max) per kilogram of body weight is two- to threefold that in humans; the difference cannot be explained solely by differences in structural features between species. We compared the functional recruitment of pulmonary diffusing capacity (DLCO) during exercise in dogs with that in humans to determine whether pulmonary gas exchange is matched to VO2max or the size of the lungs and to define the potential role of exercise-induced polycythemia in producing the superior aerobic capacity of the dogs. We compared the relationships of DLCO, membrane diffusing capacity (DMCO), and pulmonary capillary blood volume (Vc) with respect to pulmonary blood flow (Qc) by a rebreathing method during steady-state exercise in adult male human subjects and in conditioned adult male foxhounds. The slopes and intercepts of the relationships of DLCO and DMCO to Qc are significantly greater in dogs than in humans; the slopes of the relationship of Vc to Qc are similar. In dogs diffusive pulmonary gas transport is matched to the higher VO2max. The enhanced recruitment of DLCO and DMCO in dogs during exercise could potentially be explained entirely by the exercise-induced polycythemia, which is seen in dogs but not in humans.
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35

Felici, M., M. Filoche, and B. Sapoval. "Diffusional screening in the human pulmonary acinus." Journal of Applied Physiology 94, no. 5 (2003): 2010–16. http://dx.doi.org/10.1152/japplphysiol.00913.2002.

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In the mammalian lung acini, O2 diffuses into quasi-static air toward the alveolar membrane, where the gas exchange with blood takes place. The O2 flux is then influenced by the O2diffusivity, the membrane permeability, and the acinus geometric complexity. This phenomenon has been recently studied in an abstract geometric model of the acinus, the Hilbert acinus (Sapoval B, Filoche M, and Weibel ER, Proc Natl Acad Sci USA 99: 10411, 2002). This is extended here to a more realistic geometry originated from the morphological model of Kitaoka et al. (Kitaoka K, Tamura S, and Takaki R, J Appl Physiol 88: 2260–2268, 2000). Two-dimensional numerical simulations of the steady-state diffusion equation with mixed boundary conditions are used to quantify the process. The alveolar O2 concentration, or partial pressure, and the O2 flux are computed and show that diffusional screening exists at rest. These results confirm that smaller acini are more efficient, as suggested for the Hilbert acini.
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36

Wu, Qian, Lingshan Zhong, Hongwei Li, et al. "A Follow-Up Study of Lung Function and Chest Computed Tomography at 6 Months after Discharge in Patients with Coronavirus Disease 2019." Canadian Respiratory Journal 2021 (February 13, 2021): 1–7. http://dx.doi.org/10.1155/2021/6692409.

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We aimed to investigate changes in pulmonary function and computed tomography (CT) findings in patients with coronavirus disease 2019 (COVID-19) during the recovery period. COVID-19 patients underwent symptom assessment, pulmonary function tests, and high-resolution chest CT 6 months after discharge from the hospital. Of the 54 patients enrolled, 31 and 23 were in the moderate and severe group, respectively. The main symptoms 6 months after discharge were fatigue and exertional dyspnea, experienced by 24.1% and 18.5% of patients, respectively, followed by smell and taste dysfunction (9.3%) and cough (5.6%). One patient dropped out of the pulmonary function tests. Of the remaining 54 patients, 41.5% had pulmonary dysfunction. Specifically, 7.5% presented with restrictive ventilatory dysfunction (forced vital capacity <80% of the predicted value), 18.9% presented with small airway dysfunction, and 32.1% presented with pulmonary diffusion impairment (diffusing capacity for carbon monoxide <80% of the predicted value). Of the 54 patients enrolled, six patients dropped out of the chest CT tests. Eleven of the remaining 48 patients presented with abnormal lung CT findings 6 months after discharge. Patients with residual lung lesions were more common in the severe group (52.6%) than in the moderate group (3.4%); a higher proportion of patients had involvement of both lungs (42.1% vs. 3.4%) in the severe group. The residual lung lesions were mainly ground-glass opacities (20.8%) and linear opacities (14.6%). Semiquantitative visual scoring of the CT findings revealed significantly higher scores in the left, right, and both lungs in the severe group than in the moderate group. COVID-19 patients 6 months after discharge mostly presented with fatigue and exertional dyspnea, and their pulmonary dysfunction was mostly characterized by pulmonary diffusion impairment. As revealed by chest CT, the severe group had a higher prevalence of residual lesions than the moderate group, and the residual lesions mostly manifested as ground-glass opacities and linear opacities.
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Bouwsema, Melissa M., Vincent Tedjasaputra, and Michael K. Stickland. "Are there sex differences in the capillary blood volume and diffusing capacity response to exercise?" Journal of Applied Physiology 122, no. 3 (2017): 460–69. http://dx.doi.org/10.1152/japplphysiol.00389.2016.

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Previous work suggests that women may exhibit a greater respiratory limitation in exercise compared with height-matched men. Diffusion capacity (DlCO) increases with incremental exercise, and the smaller lungs of women may limit membrane diffusing capacity (Dm) and pulmonary capillary blood volume (Vc) in response to the increased oxygen demand. We hypothesized that women would have lower DlCO, DlCO relative to cardiac output (DlCO/Q̇), Dm, Vc, and pulmonary transit time, secondary to lower Vc at peak exercise. Sixteen women (112 ± 12% predicted relative V̇o2peak) and sixteen men (118 ± 22% predicted relative V̇o2peak) were matched for height and weight. Hemoglobin-corrected diffusing capacity (DlCO), Vc, and Dm were determined via the multiple-[Formula: see text] DlCO technique at rest and during incremental exercise up to 90% of V̇o2peak. Both groups increased DlCO, Vc, and Dm with exercise intensity, but women had 20% lower DlCO ( P < 0.001), 18% lower Vc ( P = 0.002), and 22% lower Dm ( P < 0.001) compared with men across all workloads, and neither group exhibited a plateau in Vc. When expressed relative to alveolar volume (Va), the between-sex difference was eliminated. The drop in DlCO/Q̇ was proportionally less in women than men, and mean pulmonary transit time did not drop below 0.3 s in either group. Women demonstrate consistently lower DlCO, Vc, and Dm compared with height-matched men during exercise; however, these differences disappear with correction for lung size. These results suggest that after differences in lung volume are accounted for there is no intrinsic sex difference in the DlCO, Vc, or Dm response to exercise. NEW & NOTEWORTHY Women demonstrate lower diffusing capacity-to-cardiac output ratio (DlCO/Q̇), pulmonary capillary blood volume (Vc), and membrane diffusing capacity (Dm) compared with height-matched men during exercise. However, these differences disappear after correction for lung size. The drop in DlCO/Q̇ was proportionally less in women, and pulmonary transit time did not drop below 0.3 s in either group. After differences in lung volume are accounted for, there is no intrinsic sex difference in DlCO, Vc, or Dm response to exercise.
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38

Usuda, Katsuo, Shun Iwai, Aika Yamagata, et al. "How to Discriminate Lung Cancer From Benign Pulmonary Nodules and Masses? Usefulness of Diffusion-Weighted Magnetic Resonance Imaging With Apparent Diffusion Coefficient and Inside/Wall Apparent Diffusion Coefficient Ratio." Clinical Medicine Insights: Oncology 15 (January 2021): 117955492110148. http://dx.doi.org/10.1177/11795549211014863.

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Background: Although diffusion-weighted imaging (DWI) is useful for differential diagnosis between lung cancers and benign pulmonary nodules and masses (BPNMs), it is difficult to differentiate pulmonary abscesses from lung cancers because pulmonary abscesses show restricted diffusion. With this research we will present how to assess the total apparent diffusion coefficient (ADC) and inside/wall ADC ratio for these pulmonary nodules and masses (PNMs). Methods: The pulmonary lesions were divided into next 3 groups. There were 40 lung cancers, 41 inflammatory benign PNMs (mycobacteria disease 13, pneumonia 12, pulmonary abscess 10, other 6) and 7 noninflammatory benign PNMs. Definitions were as follows: wall ADC = ADC value in outer one-third of the lesion; inside ADC = ADC value in central two-thirds of the lesion: inside/wall ADC ratio = ratio of inside ADC/wall ADC. Results: Mean total ADC (1.26 ± 0.32 × 10−3 mm2/s) of the lung cancers was remarkably lower than that (1.53 ± 0.53) of the BPNMs. The mean total ADC values were 1.26 ± 0.32 in lung cancer, 1.45 ± 0.47 in inflammatory BPNM and 2.04 ± 0.63 in noninflammatory BPNM, and there were significant differences among them. The mean inside ADC value (1.33 ± 0.32) of the lung cancers was remarkably higher than that (0.94 ± 0.42) of the pulmonary abscesses. The mean inside/wall ADC ratio (1.20 ± 0.28) of the lung cancers was remarkably higher than that (0.74 ± 0.14) of the pulmonary abscesses. Conclusions: Although ADC of DWI could differentiate lung cancer from BPNM, the inside/wall ADC ratio of DWI is efficient for differentiation between lung cancer and lung abscess. The inside/wall ADC ratio of DWI strengthens a weak point of DWI.
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39

Yilmaz, Cuneyt, Priya Ravikumar, Dennis J. Bellotto, Roger H. Unger, and Connie C. W. Hsia. "Fatty diabetic lung: functional impairment in a model of metabolic syndrome." Journal of Applied Physiology 109, no. 6 (2010): 1913–19. http://dx.doi.org/10.1152/japplphysiol.00549.2010.

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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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40

Prisk, G. K., H. J. Guy, A. R. Elliott, R. A. Deutschman, and J. B. West. "Pulmonary diffusing capacity, capillary blood volume, and cardiac output during sustained microgravity." Journal of Applied Physiology 75, no. 1 (1993): 15–26. http://dx.doi.org/10.1152/jappl.1993.75.1.15.

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We measured pulmonary diffusing capacity (DL), diffusing capacity per unit lung volume, pulmonary capillary blood volume (Vc), membrane diffusing capacity (Dm), pulmonary capillary blood flow or cardiac output (Qc), and cardiac stroke volume (SV) in four subjects exposed to 9 days of microgravity (weightlessness, 0 G). The same subjects were studied standing and supine numerous times preflight and in the week immediately after return from space. DL in microgravity was elevated (28%) compared with preflight standing values and was higher than preflight supine because of the elevation of both Vc (28%) and Dm (27%). The elevation in Vc was comparable to that measured supine in 1 G, but the increase in Dm was in sharp contrast to the supine value (which was unchanged). We postulate that, in 0 G, pulmonary capillary blood is evenly distributed throughout the lung, providing for uniform capillary filling, leading to an increase in the surface area available for diffusion. By contrast, in the supine 1-G state, the capillaries are less evenly filled, and although a similar increase in blood volume is observed, the corresponding increase in surface area does not occur. DL and its subdivisions showed no adaptive changes from the first measurement 24 h after the start of 0 G to 8 days later. Similarly, there were no trends in the postflight data, suggesting that the principal mechanism of these changes was gravitational. The increase in Dm suggests that subclinical pulmonary edema did not result from exposure to 0 G. Qc was modestly increased (18%) inflight and decreased (9%) post-flight compared with preflight standing. Compared with preflight standing, SV was increased 46% inflight and decreased 14% in the 1st wk postflight. There were temporal changes in Qc and SV during 0 G, with the highest values recorded at the first measurement, 24 h into the flight. The lowest values of Qc and SV occurred on the day of return.
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41

Hofemeier, Philipp, and Josué Sznitman. "Revisiting pulmonary acinar particle transport: convection, sedimentation, diffusion, and their interplay." Journal of Applied Physiology 118, no. 11 (2015): 1375–85. http://dx.doi.org/10.1152/japplphysiol.01117.2014.

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It is largely acknowledged that inhaled particles ranging from 0.001 to 10 μm are able to reach and deposit in the alveolated regions of the lungs. To date, however, the bulk of numerical studies have focused mainly on micrometer-sized particles whose transport kinematics are governed by convection and sedimentation, thereby capturing only a small fraction of the wider range of aerosols leading to acinar deposition. Too little is still known about the local acinar transport dynamics of inhaled (ultra)fine particles affected by diffusion and convection. Our study aims to fill this gap by numerically simulating the transport characteristics of particle sizes spanning three orders of magnitude (0.01-5 μm) covering diffusive, convective, and gravitational aerosol motion across a multigenerational acinar network. By characterizing the deposition patterns as a function of particle size, we find that submicrometer particles [[Formula: see text] (0.1 μm)] reach deep into the acinar structure and are prone to deposit near alveolar openings; meanwhile, other particle sizes are restricted to accessing alveolar cavities in proximal generations. Our findings underline that a precise understanding of acinar aerosol transport, and ultrafine particles in particular, is contingent upon resolving the complex convective-diffusive interplay in determining their irreversible kinematics and local deposition sites.
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42

Schulz, H., P. Heilmann, A. Hillebrecht, et al. "Convective and diffusive gas transport in canine intrapulmonary airways." Journal of Applied Physiology 72, no. 4 (1992): 1557–62. http://dx.doi.org/10.1152/jappl.1992.72.4.1557.

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The significance of convective and diffusive gas transport in the respiratory system was assessed from the response of combined inert gas and particle boluses inhaled into the conducting airways. Particles, considered as “nondiffusing gas,” served as tracers for convection and two inert gases with widely different diffusive characteristics (He and SF6) as tracers for convection and diffusion. Six-milliliter boluses labeled with monodisperse di-2-ethylhexyl sebacate droplets of 0.86-microns aerodynamic diameter, 2% He, and 2% SF6 were inspired by three anesthetized mechanically ventilated beagle dogs to volumetric lung depths up to 170 ml. Mixing between inspired and residual air caused dispersion of the inspired bolus, which was quantified in terms of the bolus half-width. Dispersion of particles increased with increasing lung depth to which the boluses were inhaled. The increase followed a power law with exponents less than 0.5 (mean 0.39), indicating that the effect of convective mixing per unit volume was reduced with depth. Within the pulmonary dead space, the behavior of the inert gases He and SF6 was similar to that of the particles, suggesting that gas transport was almost solely due to convection. Beyond the dead space, dispersion of He and SF6 increased more rapidly than dispersion of particles, indicating that diffusion became significant. The gas and particle bolus technique offers a suitable approach to differential analysis of gas transport in intrapulmonary airways of lungs.
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43

Hsia, Connie C. W., Peter D. Wagner, D. Merrill Dane, Harrieth E. Wagner, and Robert L. Johnson. "Predicting diffusive alveolar oxygen transfer from carbon monoxide-diffusing capacity in exercising foxhounds." Journal of Applied Physiology 105, no. 5 (2008): 1441–47. http://dx.doi.org/10.1152/japplphysiol.01328.2007.

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Although lung diffusing capacity for carbon monoxide (DlCO) is a widely used test of diffusive O2 transfer, few studies have directly related DlCO to O2-diffusing capacity (DlO2); none has used the components of DlCO, i.e., conductance of alveolar membrane and capillary blood, to predict DlO2 from rest to exercise. To understand the relationship between DlCO and DlO2 at matched levels of cardiac output, we analyzed cumulative data from rest to heavy exercise in 43 adult dogs, with normal lungs or reduced lung capacity following lung resection, that were studied by two techniques. 1) A rebreathing (RB) technique was used to measure DlCO and pulmonary blood flow at two O2 tensions, independent of O2 exchange. DlCO was partitioned into CO-diffusing capacity of alveolar membrane and pulmonary capillary blood volume using the Roughton-Forster equation and converted into an equivalent DlO2, [DlO2(RB)]. 2) A multiple inert-gas elimination technique (MIGET) was used to measure ventilation-perfusion distributions, O2 and CO2 exchange under hypoxia, to derive DlO2 [DlO2(MIGET)] by the Lilienthal-Riley technique and Bohr integration. For direct comparisons, DlO2(RB) was interpolated to the cardiac output measured by the Fick principle corresponding to DlO2(MIGET). The DlO2-to-DlCO ratio averaged 1.61. Correlation between DlO2(RB) and DlO2(MIGET) was similar in normal and post-resection groups. Overall, DlO2(MIGET) = 0.975 DlO2(RB); mean difference between the two techniques was under 5% for both animal groups. We conclude that, despite various uncertainties inherent in these two disparate methods, the Roughton-Forster equation adequately predicts diffusive O2 transfer from rest to heavy exercise in canines with normal, as well as reduced, lung capacities.
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44

Wagner, Peter D. "Operation Everest II and the 1978 Habeler/Messner ascent of Everest without bottled O2: what might they have in common?" Journal of Applied Physiology 123, no. 6 (2017): 1682–88. http://dx.doi.org/10.1152/japplphysiol.00140.2017.

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In 1978, Peter Habeler and Reinhold Messner climbed Everest without supplemental O2. Subsequently, Oelz et al. (Oelz O, Howald H, Di Prampero PE, Hoppeler H, Claassen H, Jenni R, Bühlmann A, Ferretti G, Brückner JC, Veicsteinas A, Gussoni M, Cerretelli P. J Appl Physiol (1985) 60: 1734–1742, 1986) assessed their cardiopulmonary function, finding no advantageous physiological attributes to explain their success, and leading West (West JB. High Life: A History of High-Altitude Physiology and Medicine. New York: Oxford University, 1998) to suggest that grit and determination were more important. In 1985, Charlie Houston, John Sutton, and Al Cymerman hosted a scientific project assessing a simulated ascent of Everest (OE II) at the U.S. Army Research Institute of Environmental Medicine. Included were measurements of O2 transport. In particular, mixed venous Po2 was measured at/near maximal exercise, for calculating pulmonary O2-diffusing capacity. A serendipitous observation was made: while both V̇o2max and mixed venous Po2 fell with altitude (as expected), it was how they fell—in direct proportion—that was remarkable. It later became clear that this reflected diffusion limitation of O2 transport from muscle microvessels to the mitochondria, and that this last step in O2 transport plays a major role in limiting V̇o2max. Thus, how Habeler and Messner made it up Everest without bottled O2 and no special cardiopulmonary attributes might be explained if their muscle O2-diffusing capacity, which depends largely on muscle capillarity, was unusually high. Oelz et al. mention that muscle capillary density was substantially—40%—above normal, but did not suggest that this accounted for the climbersʼ success. Therefore, high muscle capillarity, enhancing diffusive unloading of O2, may have been a major enabling physiological attribute for Habeler and Messner and that OE II, by chance, played a key role in bringing this to light.
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45

Bombina, L. K. "A comprehensive non-invasive method for assessing heart and lung damage in systemic scleroderma." Kazan medical journal 66, no. 2 (1985): 159–60. http://dx.doi.org/10.17816/kazmj61218.

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46

Das, Sushant Kumar, Dong Jun Yang, Jin Liang Wang, Chuan Zhang, and Han Feng Yang. "Non-Gaussian diffusion imaging for malignant and benign pulmonary nodule differentiation: a preliminary study." Acta Radiologica 58, no. 1 (2016): 19–26. http://dx.doi.org/10.1177/0284185116639763.

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Background Diffusion-weighted imaging (DWI) derived apparent diffusion coefficient (ADC) has demonstrated inconsistent results in pulmonary nodule differentiation. Diffusion kurtosis imaging (DKI), which quantifies non-Gaussian diffusion, is believed to better characterize tissue micro-structure than conventional DWI. Purpose To assess the feasibility of DKI in human lungs and to compare its diagnostic value with standard DWI in differentiating malignancies from benign pulmonary nodules. Material and Methods Thirty-five pulmonary nodules in 32 consecutive patients were evaluated by DKI by using 3b-values of 0, 500, and 1000 s/mm2 and conventional DWI with b values of 0 and 800 s/mm2. Two observers independently evaluated and compared diagnostic accuracy of mean kurtosis (MK) and ADC values in differentiating malignancies from benign pulmonary nodules. The intra- and inter-observer repeatability (intra-class correlation coefficient [ICC]) were also assessed for each derived measures. Results The diagnostic accuracy, and the area under curve (AUC) in differentiating malignancies from benign pulmonary nodule, were not significantly higher for MK (Obs. 1a: 85.70%, 0.87; Obs. 1b: 80.00%, 0.80; and Obs. 2: 82.80%, 0.91) as compared to ADC (Obs. 1a: 77.14%, 0.81; Obs. 1b: 80.00%, 0.85; and Obs. 2: 77.14%, 0.85 respectively). The intra- and inter-observer agreement (ICC) for malignant and benign lesions was substantial for each reading. Conclusion The initial results of this study indicate the feasibility of DKI in human lungs. However, there was no significant benefit of DKI derived MK values over ADC for malignant and benign pulmonary nodule differentiation.
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47

de Bisschop, Claire, Jean-Benoit Martinot, Gil Leurquin-Sterk, Vitalie Faoro, Hervé Guénard, and Robert Naeije. "Improvement in lung diffusion by endothelin A receptor blockade at high altitude." Journal of Applied Physiology 112, no. 1 (2012): 20–25. http://dx.doi.org/10.1152/japplphysiol.00670.2011.

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Lung diffusing capacity has been reported variably in high-altitude newcomers and may be in relation to different pulmonary vascular resistance (PVR). Twenty-two healthy volunteers were investigated at sea level and at 5,050 m before and after random double-blind intake of the endothelin A receptor blocker sitaxsentan (100 mg/day) vs. a placebo during 1 wk. PVR was estimated by Doppler echocardiography, and exercise capacity by maximal oxygen uptake (V̇o2 max). The diffusing capacities for nitric oxide (DLNO) and carbon monoxide (DLCO) were measured using a single-breath method before and 30 min after maximal exercise. The membrane component of DLCO (Dm) and capillary volume (Vc) was calculated with corrections for hemoglobin, alveolar volume, and barometric pressure. Altitude exposure was associated with unchanged DLCO, DLNO, and Dm but a slight decrease in Vc. Exercise at altitude decreased DLNO and Dm. Sitaxsentan intake improved V̇o2 max together with an increase in resting and postexercise DLNO and Dm. Sitaxsentan-induced decrease in PVR was inversely correlated to DLNO. Both DLCO and DLNO were correlated to V̇o2 max at sea level ( r = 0.41–0.42, P < 0.1) and more so at altitude ( r = 0.56–0.59, P < 0.05). Pharmacological pulmonary vasodilation improves the membrane component of lung diffusion in high-altitude newcomers, which may contribute to exercise capacity.
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48

Idorn, Lars, Birgitte Hanel, Annette S. Jensen, et al. "New insights into the aspects of pulmonary diffusing capacity in Fontan patients." Cardiology in the Young 24, no. 2 (2013): 311–20. http://dx.doi.org/10.1017/s1047951113000358.

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AbstractBackground: Patients with a functionally univentricular heart, palliated a.m. Fontan, consequently have non-pulsatile pulmonary blood flow and are known to have a reduced pulmonary diffusing capacity. However, the cause of this reduction remains unclear. We aimed to assess the possible determinants in the aetiology of a reduced diffusing capacity and also to assess whether it could be increased. Furthermore, we aimed to search for predictors of a reduced diffusing capacity. Material and methods: A total of 87 Fontan patients (mean age 16.3 ± 7.6 years) performed advanced pulmonary function tests and maximal cycle ergometer tests. A total of 10 Fontan patients and nine matched controls performed a supine pulmonary function test after a supine rest. Results: In the sitting pulmonary function test, the mean z-scores were: diffusing capacity, 2.38 ± 1.20; pulmonary capillary blood volume, 2.04 ± 0.80; and alveolar capillary membrane diffusing capacity, 0.14 ± 0.84. In the supine compared with the sitting pulmonary function test, the diffusing capacity increased by 51.7 ± 11.9% in the Fontan group and by 23.3 ± 17.7% in the control group (p < 0.001); moreover, the pulmonary capillary blood volume increased by 48.3 ± 17.4% in the Fontan group and by 20.2 ± 13.9% in the control group (p = 0.001). In a multiple linear regression analysis including the explanatory variables of surgical data and exercise data at rest and peak exercise, the resting cardiac index was an independent predictor of the diffusing capacity (regression coefficient: 0.18, p < 0.001). Conclusions: The pulmonary diffusing capacity was reduced in Fontan patients because of a reduced pulmonary capillary blood volume, whereas the alveolar capillary membrane diffusing capacity was preserved. The diffusing capacity was highly increasable in Fontan patients compared with controls, and the resting cardiac index was an independent predictor of the diffusing capacity.
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Ningsih, Ririn Astuty, Faisal Yunus, Triya Damayanti, et al. "Lung Diffusion Capacity of X Fighter Pilot in Madiun." Jurnal Respirologi Indonesia 40, no. 1 (2020): 39–47. http://dx.doi.org/10.36497/jri.v40i1.96.

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Background: Pilot works in the high environment that exposed by G force. Increasing G force led to linear decreases in cardiac output and blood oxygenation of the brain. Thus, likely due to decreased lung gas exchange capacity in hypergravity. This study aims to investigate the pulmonary diffusing capacity test among Fighter pilots in Madiun. 
 Methods: This study used cross sectional method conducted on February 2019 in Madiun. The total subjects consist of 44 Fighter pilots based on total sampling. Interview was done to fill out question about sociodemografic and smoking habit, flight hour data and physical fitness. Lung function measurement was done using portable spirometry and DLCO equipment (Easyone TM Pro Lab). 
 Result: Spirometri result was found in the standard normal range in 41 subjects (93,2%) only 3 subject (6,8%) get obstruction abnormalities and none of them get restriction result. Average VEP1 prediction was 103,3±10,60 % and median range for VEP1/KVP was 84,5(63,5-92,5) %. Lung diffusion capacity measurement was found to be normal in 41 subject (93,2%) and to be deficient in 3 subject (6,8%) in smoker.
 Conclusion: This study demosntrated that diffusion capacity and spirometry test in Fighter pilots generally in normal range. Lung diffusion capacity has no association with age, BMI, flight hour, physical fitness, Brinkman index and spirometry parameters. (J Respir Indo. 2020; 40(1): 39-47)
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Merrikh, Ali A., and José L. Lage. "Effect of Blood Flow on Gas Transport in a Pulmonary Capillary." Journal of Biomechanical Engineering 127, no. 3 (2004): 432–39. http://dx.doi.org/10.1115/1.1894322.

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The effects of blood velocity on gas transport within the alveolar region of lungs, and on the lung diffusing capacity DL have for many years been regarded as negligible. The present work reports on a preliminary, two-dimensional investigation of CO convection-diffusion phenomenon within a pulmonary capillary. Numerical simulations were performed using realistic clinical and morphological parameter values, with discrete circular red blood cells (RBCs) moving with plasma in a single capillary. Steady-state simulations with stationary blood (RBCs and plasma) were performed to validate the model by comparison with published data. Results for RBCs moving at speeds varying from 1.0mm∕s to 10mm∕s, and for capillary hematocrit (Ht) from 5% to 55%, revealed an increase of up to 60% in DL, as compared to the stationary blood case. The increase in DL is more pronounced at low Ht (less than 25%) and high RBC speed and it seems to be caused primarily by the presence of plasma. The results also indicate that capillary blood convection affects DL not only by improving the plasma mixing in the capillary bed but also by replenishing the capillary with fresh (zero concentration) plasma, providing an additional reservoir for the consumption of CO. Our findings cast doubt on the current belief that an increase in the lung diffusing capacity of humans (for instance, during exercising), with fixed hematocrit, can only be accomplished by an increase in the lung volume effectively active in the respiration process.
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