scholarly journals Development of lung diffusion to adulthood following extremely preterm birth

2021 ◽  
pp. 2004103
Author(s):  
Emma Satrell ◽  
Hege Clemm ◽  
Ola Røksund ◽  
Karl Ove Hufthammer ◽  
Einar Thorsen ◽  
...  

BackgroundGas exchange in extremely preterm (EP) infants must take place in foetal lungs. Childhood lung diffusing capacity for carbon monoxide (DLCO) is reduced; however, longitudinal development has not been investigated. We describe growth of DLCO and its sub-components to adulthood in EP-born compared to term-born subjects.MethodsTwo area-based cohorts born at gestational age ≤28 weeks or birth weight ≤1000 grams in 1982–1985 (n=48) and 1991–1992 (n=35) were examined twice, at ages 18 and 25, and 10 and 18 years, respectively, and compared to matched term-born controls. Single-breath DLCO was measured at two oxygen pressures, with sub-components [membrane diffusion (DM) and pulmonary capillary blood volume (VC)] calculated using the Roughton–Forster equation.ResultsAge-, sex- and height-standardized transfer coefficients for carbon monoxide (KCO), and DLCO were reduced in EP-born compared to term-born and remained so during puberty and early adulthood (p-values for all time points and both cohorts ≤0.04), whereas alveolar volume was similar. Development occurred in parallel to term-born controls, with no signs of pubertal catch-up growth nor decline at 25 years (p-values for lack of parallelism within cohorts 0.99, 0.65, 0.71, 0.94, and 0.44 for z-DLCO, z-VA, z-KCO, DM, and VC, respectively). Split by membrane and blood volume components, findings were less clear; however, membrane diffusion seemed most affected.ConclusionPulmonary diffusing capacity was reduced in EP-born compared to term-born, and development from childhood to adulthood tracked in parallel to term-born, with no signs of catch-up growth nor decline at age 25.

2008 ◽  
Vol 104 (4) ◽  
pp. 1094-1100 ◽  
Author(s):  
Sylvia Verbanck ◽  
Daniel Schuermans ◽  
Sophie Van Malderen ◽  
Walter Vincken ◽  
Bruce Thompson

It has long been assumed that the ventilation heterogeneity associated with lung disease could, in itself, affect the measurement of carbon monoxide transfer factor. The aim of this study was to investigate the potential estimation errors of carbon monoxide diffusing capacity (DlCO) measurement that are specifically due to conductive ventilation heterogeneity, i.e., due to a combination of ventilation heterogeneity and flow asynchrony between lung units larger than acini. We induced conductive airway ventilation heterogeneity in 35 never-smoker normal subjects by histamine provocation and related the resulting changes in conductive ventilation heterogeneity (derived from the multiple-breath washout test) to corresponding changes in diffusing capacity, alveolar volume, and inspired vital capacity (derived from the single-breath DlCO method). Average conductive ventilation heterogeneity doubled ( P < 0.001), whereas DlCO decreased by 6% ( P < 0.001), with no correlation between individual data ( P > 0.1). Average inspired vital capacity and alveolar volume both decreased significantly by, respectively, 6 and 3%, and the individual changes in alveolar volume and in conductive ventilation heterogeneity were correlated ( r = −0.46; P = 0.006). These findings can be brought in agreement with recent modeling work, where specific ventilation heterogeneity resulting from different distributions of either inspired volume or end-expiratory lung volume have been shown to affect DlCO estimation errors in opposite ways. Even in the presence of flow asynchrony, these errors appear to largely cancel out in our experimental situation of histamine-induced conductive ventilation heterogeneity. Finally, we also predicted which alternative combination of specific ventilation heterogeneity and flow asynchrony could affect DlCO estimate in a more substantial fashion in diseased lungs, irrespective of any diffusion-dependent effects.


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


1985 ◽  
Vol 68 (1) ◽  
pp. 57-62 ◽  
Author(s):  
J. A. Wedzicha ◽  
F. E. Cotter ◽  
P. J. W. Wallis ◽  
A. C. Newland ◽  
D. W. Empey

1. The transfer factor for carbon monoxide and its subdivisions, the membrane diffusing capacity (Dm) and the pulmonary capillary blood volume (Vc), were measured in 16 patients with polycythaemia secondary to chronic hypoxic lung disease and in ten hypoxic non-polycythaemic control subjects. 2. The mean pulmonary capillary blood volume was significantly lower in the polycythaemic patients (31.6 ml, sd 11.2) compared with the control group (65.2 ml, sd 22.5) (P<0.001). 3. Erythrapheresis, as a method of isovolaemic haemodilution, was performed in 15 of the polycythaemic patients. The mean packed cell volume fell from 58 (sd 5)% to 47 (sd 5)% after treatment, with significant reductions in blood viscosity at both high and lower shear rates (P<0.001). 4. The mean pulmonary capillary blood volume increased from 32.3 ml (sd 11.3) before treatment to 48.7 ml (sd 18.7) after erythrapheresis (P<0.01), with no significant change in membrane diffusing capacity. 5. The rise in pulmonary capillary blood volume is another potential physiological advantage of the reduction of packed cell volume in patients with polycythaemia secondary to hypoxic lung disease.


2020 ◽  
pp. 00567-2020
Author(s):  
Natalie Terzikhan ◽  
Hanfei Xu ◽  
Ahmed Edris ◽  
Ken R. Bracke ◽  
Fien M. Verhamme ◽  
...  

BackgroundEpigenetics may play an important role in pathogenesis of lung diseases. However, little is known about the epigenetic factors that influence impaired gas exchange at the lungs.AimTo identify the epigenetic signatures of the diffusing capacity of the lung measured by carbon monoxide uptake.MethodsEpigenome-Wide Association Study (EWAS) was performed on diffusing capacity, measured by carbon monoxide uptake (DLCO) and per alveolar volume (DLCO /VA) using the single-breath technique in 2674 individuals from two population-based cohort studies, the Rotterdam Study (the discovery panel) and the Framingham Heart Study (the replication panel). We assessed the clinical relevance of our findings by investigating the identified sites in whole blood and lung tissue specific gene expression.ResultsWe identified and replicated two CpG sites (cg05575921 and cg05951221) that were significantly associated with DLCO /VA and one (cg05575921) suggestively associated with DLCO. Furthermore, we found a positive association between AHRR (cg05575921) hypomethylation and gene expression of EXOC3 in whole blood. We confirmed that the expression of EXOC3 in lung tissue is positively associated with DLCO/VA and DLCO.ConclusionsWe report on epigenome wide associations with diffusing capacity in the general population. Our results suggest EXOC3 to be an excellent candidate through which smoking induced hypomethylation of AHRR might affect pulmonary gas exchange.


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