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Regional pulmonary deformation is positively correlated with regional lung inflammation assessed by 18F-FDG positron emission tomography / computed tomography
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
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(English)Manuscript (preprint) (Other academic)
Abstract [en]

Objective: Lung deformation beyond of physiological capacity is associated with cell death and inflammation. Lung strain has been estimated as a global strain, but uneven strain distribution may lead to regional stress concentrations and lung damage. Local lung inflammation can be estimated using PET imaging of [18F]fluoro-2-deoxy-D-glucose. We hypothesized that local lung deformation correlates well with local inflammation. The aim of this study was to assess local tidal deformations by using a new mathematical model of finite-elements to analyze CT images, and to correlate them with local inflammation in a porcine experimental model of early acute respiratory distress syndrome.

Design: Retrospective images analysis, laboratory investigation.

Setting: University animal research laboratory.

Subjects: Seven piglets submitted to experimental ventilator-induced lung injury and five healthy ventilated controls.

Intervention: Lung injury was induced by repeated lung lavages and 210 minutes of injurious mechanical ventilation using low positive end-expiratory pressure and high inspiratory pressures. All animals were subsequently studied with dynamic PET imaging of [18F]fluoro-2-deoxy-D-glucose. CT scans were acquired at end expiration and end inspiration. Then maps of deformation were constructed and regional deformation was estimated. We divided the lung parenchyma in 10 horizontal ROIs, and correlations of local volumetric strain and [18F]fluoro-2-deoxy-D-glucose uptake were analyzed in each ROI.

Measurements and Main Results: The deformation maps showed a heterogeneous distribution with a greater concentration in the intermediate gravitational regions. We found a strong correlation between local strain and inflammation (R2 > 0.5) for the whole lung, when we eliminate the 3/10 dorsal ROIs R2 increased until>0.8.

Conclusion: the present findings suggest that the greater local stretches were mainly concentrated in the intermediate gravitational zones of injured heterogeneous lungs. Additionally, local lung deformations correlated well with local inflammation in this experimental model of VILI. And the new proposed image-based estimation of regional volumetric strain based on finite element interpolations has the potential to give new insights of local pathogenic mechanisms of VILI and how best design protective-ventilations strategies.

National Category
Anesthesiology and Intensive Care
Identifiers
URN: urn:nbn:se:uu:diva-296945OAI: oai:DiVA.org:uu-296945DiVA, id: diva2:940239
Available from: 2016-06-20 Created: 2016-06-20 Last updated: 2016-08-25Bibliographically approved
In thesis
1. Aspects on ventilation induced stress and strain on regional and global inflammation in experimental acute respiratory distress syndrome
Open this publication in new window or tab >>Aspects on ventilation induced stress and strain on regional and global inflammation in experimental acute respiratory distress syndrome
2016 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Mechanical ventilation (MV) is a life-saving therapy in acute respiratory distress syndrome (ARDS), a condition that affects 3000 patients/year in Sweden with a mortality rate of about 40%. However, MV may induce or worsen lung injury causing “ventilator-induced lung injury (VILI)”. From a mechanical perspective strain (deformation, or relative change in lung volume) and stress (tension) have been postulated as main determinants of VILI. High respiratory rate is potentially another factor that may exacerbate VILI by amplifying the total energy transmitted to the lungs during MV. In this thesis in animal ARDS models the hypotheses were that 1) lung parenchyma inhomogeneities concentrate stress and amplify lung damage and inflammation, 2) higher respiratory rates increase lung inflammation and lung edema in heterogeneous ARDS, and 3) local lung deformation is related to local inflammation.

First, in a rat model the effect on inflammation and structural damage of regional lung collapse on the healthy surrounding lung tissue was assessed. Second, in porcine models the effect of respiratory rate on lung edema and inflammation was studied during two ventilatory modes; a) a permissive collapse mode and b) a homogenized lung parenchyma mode. Finally, lung deformation was correlated with lung inflammation assessed by positron emission tomography using 18F-FDG uptake.

It was found that; 1) local inhomogeneities can act as stress amplifiers, increasing lung tissue inflammation and damage in the healthy surrounded lung. 2) high respiratory rate increases lung edema but decreases lung inflammation when permissive lung collapse is used and that these effects are prevented with lung parenchyma homogenization; 3) local lung deformation and inflammation are well correlated.

In conclusion, lung inhomogeneities may aggravate VILI, respiratory rate may affect in different ways VILI progression depending on the ventilatory strategy, and finally, lung deformation is closely related to lung inflammation. With the caveat that the studies are performed in animal models, the results suggest that using ventilator strategies that homogenize the lungs, i.e., open collapsed lung regions and prevent re-collapse in ARDS will reduce VILI and in the end may decrease morbidity and the high mortality in this condition.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2016. p. 64
Series
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 1235
Keywords
ARDS, VILI, respiratory rate, strain, PET
National Category
Anesthesiology and Intensive Care
Identifiers
urn:nbn:se:uu:diva-296952 (URN)978-91-554-9612-8 (ISBN)
External cooperation:
Public defence
2016-09-06, Hedstrandsalen, Akademiska sjukhuset, Ing 70, 751 85 Uppsala, UPPSALA, 09:00 (English)
Opponent
Supervisors
Funder
Swedish Heart Lung Foundation, K2015-99X-22731-01-4
Available from: 2016-08-16 Created: 2016-06-20 Last updated: 2016-08-25

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