Respiratory illnesses, such as bronchitis, emphysema, asthma, and COVID-19, substantially remodel lung tissue, deteriorate function, and culminate in a compromised breathing ability. Yet, the structural mechanics of the lung is significantly understudied. Classical pressure-volume air or saline inflation studies of the lung have attempted to characterize the organ’s elasticity and compliance, measuring deviatory responses in diseased states; however, these investigations are exclusively limited to the bulk composite or global response of the entire lung and disregard local expansion and stretch phenomena within the lung lobes, overlooking potentially valuable physiological insights, as particularly related to mechanical ventilation. Here, we present a method to collect the first non-contact, full-field deformation measures of ex vivo porcine and murine lungs and interface with a pressure-volume ventilation system to investigate lung behavior in real time. We share preliminary observations of heterogeneous and anisotropic strain distributions of the parenchymal surface, associative pressure-volume-strain loading dependencies during continuous loading, and consider the influence of inflation rate and maximum volume. This study serves as a crucial basis for future works to comprehensively characterize the regional response of the lung across various species, link local strains to global lung mechanics, examine the effect of breathing frequencies and volumes, investigate deformation gradients and evolutionary behaviors during breathing, and contrast healthy and pathological states. Measurements collected in this framework ultimately aim to inform predictive computational models and enable the effective development of ventilators and early diagnostic strategies.
Objective Therapy for moderate ischemic mitral regurgitation (IMR) remains unclear. Determination of myocardial viability, a necessary pre-requisite for an improvement in regional contractility, is a likely key factor in determining response to revascularization alone. Myocardial strain has been proposed as a viability measure but has not been compared to late gadolinium enhancement (LGE) cardiac (c)MRI. We hypothesized that abnormal strain overestimates non-viable LV segments measured using LGE and that ischemia and mechanical tethering by adjacent transmural myocardial infarction (TMI) also decreases strain in viable segments. Methods Sixteen patients with ≥ mild IMR and seven healthy volunteers underwent cMRI with non-invasive tags (CSPAMM), LGE and stress perfusion. CSPAMM images were post-processed with HARP and circumferential and longitudinal strains were calculated. Viability was defined as the absence of TMI on LGE (hyperenhancement >50% of wall thickness). The borderzone was defined as any segment bordering TMI. Abnormal strain thresholds (±1–2.5 SD from normal mean) were compared to TMI, ischemia and borderzone. Results 7.4% of LV segments had TMI on LGE while >14.5% of LV segments were non-viable by strain thresholds (p<0.005). In viable segments, ischemia impaired longitudinal strain (least perfused 1/3 of LV segments −.18±.08 vs. most perfused −.22±.1 p=01) and circumferential strain (−.12±.1 vs−.16±.08 p<0.05). In addition, infarct proximity impaired longitudinal strain (−.16±.11 borderzone vs −.18±.09 remote p=.05). Conclusions Impaired LV strain overestimates non-viable myocardium when compared to TMI on LGE. Ischemia and infarct proximity also decrease strain in viable segments.
This is the first study to decouple the membrane-cytoskeleton elasticity from cell stiffness and introduce an effective approach for measuring the elastic modulus. The novelty of this study is the development of new technology for quantifying the elastic stiffness of the membrane-cytoskeleton system of cells. This capability could have immense implications in cell biology, particularly in establishing correlations between various cell diseases, mortality, and differentiation with membrane-cytoskeleton elasticity, examining through-tissue cell migration, and understanding cell infiltration in porous scaffolds. The present method can be further extended to analyze membrane-cytoskeleton viscous behavior, identify the contribution of other subcellular components (e.g., nucleus envelope) to load sharing, and elucidate mechanotransduction effects due to repetitive compressive loading and unloading on cell differentiation and motility.
Background Chronic ischemic mitral regurgitation (CIMR: MR) is associated with poor outcome. Left ventricular (LV) strain after postero-lateral myocardial infarction (MI) may drive LV remodeling. Although moderate CIMR has been previously shown to effect LV remodeling, the effect of CIMR on LV strain after postero-lateral MI remains unknown. We tested the hypothesis that moderate CIMR alters LV strain after postero-lateral MI. Methods/Results Postero-lateral MI was created in 10 sheep. Cardiac MRI with tags was performed 2 weeks before and 2, 8 and 16 weeks after MI. LV and right ventricular (RV) volumes were measured and regurgitant volume indexed to body surface area (BSA; RegurgVolume Index) calculated as the difference between LV and RV stroke volumes / BSA. Three-dimensional strain was calculated. Circumferential (Ecc)and longitudinal (Ell) strains were reduced in the infarct proper, MI borderzone (BZ) and remote myocardium 16 weeks after MI. In addition, radial circumferential (Erc) and radial longitudinal (Erl) shear strains were reduced in remote myocardium but increased in the infarct and BZ 16 weeks after MI. Of all strain components, however, only Erc was effected by RegurgVolume Index (p=0.0005). There was no statistically significant effect of RegurgVolume Index on Ecc, Ell, Erl, or circumferential longitudinal shear strain (Ecl). Conclusions Moderate CIMR alters radial circumferential shear strain after postero-lateral MI in the sheep. Further studies are needed to determine the effect of shear strain on myocyte hypertrophy and the effect of mitral repair on myocardial strain.
Objectives Surgical ventricular restoration (Dor procedure) is generally thought to reduce left ventricular (LV) myofiber stress (FS) but to adversely affect pump function. However, the underlying mechanism is unclear. The goal of this study was to determine the effect of residual stress (RS) on LV FS and pump function after the Dor procedure. Methods Previously described finite element models of the LV based on MRI data obtained in five sheep 16 weeks after antero-apical myocardial infarction were used. Simulated Dacron patches that were elliptical and 25% of the infarct opening area were implanted using a virtual suture technique (VIRTUAL-DOR). In each case, diastole and systole were simulated and RS, FS, LV volumes, systolic and diastolic function, and pump (Starling) function were calculated. Results VIRTUAL-DOR was associated with significant RS that was tensile (2.89±1.31 kPa) in the remote myocardium and compressive (234.15±65.53 kPa) in the borderzone (BZ). VIRTUAL-DOR+RS (compared to VIRTUAL-DOR-NO-RS) was associated with further reduction in regional diastolic and systolic FS with the greatest change in the BZ (43.5-fold and 7.1-fold respectively, p<0.0001). VIRTUAL-DOR+RS was also associated with further reduction in systolic and diastolic volumes (7.9%, p=0.0606 and 10.6%, p=0.0630, respectively). The resultant effect was a further reduction in pump function after VIRTUAL-DOR+RS. Conclusion Residual stress that occurs after the Dor procedure is positive (tensile) in the remote myocardium and negative (compressive) in the BZ and associated with reductions in fiber stress and LV volumes. The resultant effect is a further reduction in LV pump (Starling) function.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.