Aging Effects on Alveolar Sacs Under Mechanical Ventilation

Abstract

Alveolar sacs are primarily responsible for gas exchange in the human respiratory system and lose their functionality with aging. Three-dimensional (3D) models of young and old human alveolar sacs were constructed and fluid-solid interaction (FSI) was employed to investigate the contribution of age-related changes to decline in alveolar sacs function under mechanical ventilation (MV). Simulations results illustrated that compliance and pressure reduced in the alveolar sacs of the elderly, and they have to work harder to breathe. Morphological changes were found to be mainly responsible for the decline in alveolar sacs function. Influence of individual differences on the alveolar sacs function was negligible and 95% confidence intervals for compliance and WOB using measures from different individuals also support this finding. Moreover, higher mortality risk was recorded for elderly who undergo MV. Specifically, ventilator devices setting has been identified as a potential parameter for compromising respiratory function in the elderly. Volume-controlled ventilation applied less pressure, whereas, pressure-controlled ventilation resulted in higher compliance in the alveolar sacs and decreased work of breathing (WOB). Sensitivity of alveolar sacs to ventilator setting under the volume-controlled mode illustrated that increasing breathing frequency and decreasing the ratio of inhalation to exhalation times (I/E) and tidal volume (TV) caused an increase in alveolar sacs expansion and compliance in older patients. Results from this study can help clinicians to develop individualized and effective ventilator protocols and improve respiratory function in the elderly.

Characterization of air flow and lung function in the pulmonary acinus by fluid-structure interaction in idiopathic interstitial pneumonias

“…First, the surface tension of the gas-liquid interface is not included in the model. Due to the complexity of CFD and FSI simulations, many CFD or FSI studies of airway do not contain surface tension [10–12, 36], just like our research. However, the surface tension contributed a large part of the hysteresis [39, 51] and facilitate anisotropic deformation on the alveolar surface [52].…”

“…The pulmonary acinus tissue is assumed to be a hyper-elastic material in the non-linear material models. Among these models, the Neo-Hookean model is used for the tissue [35, 36]. In the FEAP code, the modified Neo-Hookean model is used, with the stored energy function is given as where the parameters K and G are equivalent to the small strain bulk and shear moduli, respectively.…”

Review of Mathematical Modeling of the Inflammatory Response in Lung Infections and Injuries

“…From smoking to COPD and in asthma, the complex interplay from molecular to tissue scales in non-infectious injuries is unclear. Many models for these types of injuries have been developed but primarily focus on biomechanics and general inflammation [54,[192][193][194][195][196][197]. However, there have been some models for non-infectious injury that have explicitly studied the immune response.…”

β-Endorphin (an endogenous opioid) inhibits inflammation, oxidative stress and apoptosis via Nrf-2 in asthmatic murine model

“…Several evidences support the direct correlation of increased oxidative stress and excessive ROS production with oxidizing biomolecules or structurally transform proteins and genes triggering different signaling cascades which might onset and advances inflammatory phenomenon in asthmatic lungs 13 . ROS and other oxides generated activate transcription factors and pro-inflammatory genes commencing inflammation leading to direct injury or inducing a variety of cellular responses 14 .…”