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The main physiological function of coughing is to remove from the airways the mucus and foreign particles that enter the lungs with respirable air. However, in patients with endotracheal tubes, further surgery has to be performed to improve cough effectiveness. Thus, it is necessary to analyze how this process is carried out in healthy tracheas to suggest ways to improve its efficacy in operated patients. A finite element model of a human trachea is developed and used to analyze the deformability of the tracheal walls under coughing. The geometry of the trachea is obtained from CT of a 70-year-old male patient. A fluid structure interaction approach is used to analyze the deformation of the wall when the fluid (in this case, air) flows inside the trachea. A structured hexahedral-based grid for the tracheal walls and an unstructured tetrahedral-based mesh with coincident nodes for the fluid are used to perform the simulations with the finite element-based commercial software code (ADINA R&D Inc.). Tracheal wall is modeled as an anisotropic fiber reinforced hyperelastic solid material in which the different orientation of the fibers is introduced. The implantation of an endotracheal prosthesis is simulated. Boundary conditions for breathing and coughing are applied at the inlet and at the outlet surfaces of the fluid mesh. The collapsibility of a human trachea under breathing and coughing is shown in terms of flow patterns and wall stresses. The ability of the model to reproduce the normal breathing and coughing is proved by comparing the deformed shape of the trachea with experimental results. Moreover the implantation of an endotracheal prosthesis would be related with a decrease of coughing efficiency, as clinically seen.

In this work, a fluid-solid interaction (FSI) analysis of a healthy and a stenotic human trachea was studied to evaluate flow patterns, wall stresses, and deformations under physiological and pathological conditions. The two analyzed tracheal geometries, which include the first bifurcation after the carina, were obtained from computed tomography images of healthy and diseased patients, respectively. A finite element-based commercial software code was used to perform the simulations. The tracheal wall was modeled as a fiber reinforced hyperelastic solid material in which the anisotropy due to the orientation of the fibers was introduced. Impedance-based pressure waveforms were computed using a method developed for the cardiovascular system, where the resistance of the respiratory system was calculated taking into account the entire bronchial tree, modeled as binary fractal network. Intratracheal flow patterns and tracheal wall deformation were analyzed under different scenarios. The simulations show the possibility of predicting, with FSI computations, flow and wall behavior for healthy and pathological tracheas. The computational modeling procedure presented herein can be a useful tool capable of evaluating quantities that cannot be assessed in vivo, such as wall stresses, pressure drop, and flow patterns, and to derive parameters that could help clinical decisions and improve surgical outcomes.

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In this work we analyzed the response of a stenotic trachea after a stent implantation. An endotracheal stent is the common treatment for tracheal diseases such as stenosis, chronic cough, or dispnoea episodes. Medical treatment and surgical techniques are still challenging due to the difficulties in overcoming potential complications after prosthesis implantation. A finite element model of a diseased and stented trachea was developed starting from a patient specific computerized tomography (CT) scan. The tracheal wall was modeled as a fiber reinforced hyperelastic material in which we modeled the anisotropy due to the orientation of the collagen fibers. Deformations of the tracheal cartilage rings and of the muscular membrane, as well as the maximum principal stresses, are analyzed using a fluid solid interaction (FSI) approach. For this reason, as boundary conditions, impedance-based pressure waveforms were computed modeling the nonreconstructed vessels as a binary fractal network. The results showed that the presence of the stent prevents tracheal muscle deflections and indicated a local recirculatory flow on the stent top surface which may play a role in the process of mucous accumulation. The present work gives new insight into clinical procedures, predicting their mechanical consequences. This tool could be used in the future as preoperative planning software to help the thoracic surgeons in deciding the optimal prosthesis type as well as its size and positioning.

A computational fluid dynamics model of a healthy, a stenotic and a post-operatory stented human trachea was developed to study the respiration under physiological boundary conditions. For this, outflow pressure waveforms were computed from patient-specific spirometries by means of a method that allows to compute the peripheral impedance of the truncated bronchial generation, modelling the lungs as fractal networks. Intratracheal flow pattern was analysed under different scenarios. First, results obtained using different outflow conditions were compared for the healthy trachea in order to assess the importance of using impedance-based conditions. The resulted intratracheal pressures were affected by the different boundary conditions, while the resulted velocity field was unaffected. Impedance conditions were finally applied to the diseased and the stented trachea. The proposed impedance method represents an attractive tool to compute physiological pressure conditions that are not possible to extract in vivo. This method can be applied to healthy, pre- and post-operatory tracheas showing the possibility of predicting, through numerical simulation, the flow and the pressure field before and after surgery.

BackgroundChronic systemic inflammatory syndrome has been implicated in the pathobiology of extrapulmonary manifestations of chronic obstructive pulmonary disease (COPD). We aimed to investigate which cell types within lung tissue are responsible for expressing major acute-phase reactants in COPD patients and disease-free (“resistant”) smokers.MethodsAn observational case–control study was performed to investigate three different cell types in surgical lung samples of COPD patients and resistant smokers via expression of the C-reactive protein (CRP) and serum amyloid A (SAA1, SAA2 and SAA4) genes. Epithelial cells, macrophages and fibroblasts from the lung parenchyma were separated by magnetic microbeads (CD326, CD14 and anti-fibroblast), and gene expression was evaluated by RT-PCR.ResultsThe sample consisted of 74 subjects, including 40 COPD patients and 34 smokers without disease. All three cell types were capable of synthesizing these biomarkers to some extent. In fibroblasts, gene expression analysis of the studied biomarkers demonstrated increased SAA2 and decreased SAA1 in patients with COPD. In epithelial cells, there was a marked increase in CRP, which was not observed in fibroblasts or macrophages. In macrophages, however, gene expression of these markers was decreased in COPD patients compared to controls.ConclusionsThese results provide novel information regarding the gene expression of CRP and SAA in different cell types in the lung parenchyma. This study revealed differences in the expression of these markers according to cell type and disease status and contributes to the identification of cell types that are responsible for the secretion of these molecules.