{"title":"Instability of vascular bilayer reveals the protective role of connective tissue","authors":"Dong Wu , Benzhu Guo , Yafei Yin , Shuai Zuo , Hongshuai Lei , Zeang Zhao , Daining Fang","doi":"10.1016/j.jmps.2025.106466","DOIUrl":null,"url":null,"abstract":"<div><div>Biological vessels are often enveloped by connective tissues that exhibit markedly different mechanical properties from the vessel wall, including high compressibility and nonlinear strain stiffening. While these composite structures are ubiquitous in soft tissue systems, the role of surrounding connective tissue in modulating vascular buckling behavior remains poorly understood. In this study, we develop a theoretical framework to investigate how connective tissue regulate mechanical stability in bilayer vessel–tissue systems. Moving beyond conventional models that assume homogeneous and incompressible materials, we introduce a more physiologically representative structure composed of a compliant, compressible outer tissue layer enclosing a stiff, incompressible vascular core. A bifurcation analysis based on incremental theory is performed to predict critical buckling performance, with results validated by both experiments and finite element simulations. The results reveal that connective tissue’s compressibility substantially increases the buckling threshold by redistributing stress across the interface and mitigating stress concentration within the vessel layer. Furthermore, comparison with actual aortic tissue reveals a stress-deconcentrating mechanism that enhances the structural resistance to buckling, a behavior not captured by idealized neoHookean models. These findings might provide mechanistic insights into tissue-mediated buckling suppression and offer design guidelines in soft biological interfaces and vascular-mimetic materials.</div></div>","PeriodicalId":17331,"journal":{"name":"Journal of The Mechanics and Physics of Solids","volume":"208 ","pages":"Article 106466"},"PeriodicalIF":6.2000,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of The Mechanics and Physics of Solids","FirstCategoryId":"5","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0022509625004405","RegionNum":2,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/12/1 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"MATERIALS SCIENCE, MULTIDISCIPLINARY","Score":null,"Total":0}
引用次数: 0
Abstract
Biological vessels are often enveloped by connective tissues that exhibit markedly different mechanical properties from the vessel wall, including high compressibility and nonlinear strain stiffening. While these composite structures are ubiquitous in soft tissue systems, the role of surrounding connective tissue in modulating vascular buckling behavior remains poorly understood. In this study, we develop a theoretical framework to investigate how connective tissue regulate mechanical stability in bilayer vessel–tissue systems. Moving beyond conventional models that assume homogeneous and incompressible materials, we introduce a more physiologically representative structure composed of a compliant, compressible outer tissue layer enclosing a stiff, incompressible vascular core. A bifurcation analysis based on incremental theory is performed to predict critical buckling performance, with results validated by both experiments and finite element simulations. The results reveal that connective tissue’s compressibility substantially increases the buckling threshold by redistributing stress across the interface and mitigating stress concentration within the vessel layer. Furthermore, comparison with actual aortic tissue reveals a stress-deconcentrating mechanism that enhances the structural resistance to buckling, a behavior not captured by idealized neoHookean models. These findings might provide mechanistic insights into tissue-mediated buckling suppression and offer design guidelines in soft biological interfaces and vascular-mimetic materials.
期刊介绍:
The aim of Journal of The Mechanics and Physics of Solids is to publish research of the highest quality and of lasting significance on the mechanics of solids. The scope is broad, from fundamental concepts in mechanics to the analysis of novel phenomena and applications. Solids are interpreted broadly to include both hard and soft materials as well as natural and synthetic structures. The approach can be theoretical, experimental or computational.This research activity sits within engineering science and the allied areas of applied mathematics, materials science, bio-mechanics, applied physics, and geophysics.
The Journal was founded in 1952 by Rodney Hill, who was its Editor-in-Chief until 1968. The topics of interest to the Journal evolve with developments in the subject but its basic ethos remains the same: to publish research of the highest quality relating to the mechanics of solids. Thus, emphasis is placed on the development of fundamental concepts of mechanics and novel applications of these concepts based on theoretical, experimental or computational approaches, drawing upon the various branches of engineering science and the allied areas within applied mathematics, materials science, structural engineering, applied physics, and geophysics.
The main purpose of the Journal is to foster scientific understanding of the processes of deformation and mechanical failure of all solid materials, both technological and natural, and the connections between these processes and their underlying physical mechanisms. In this sense, the content of the Journal should reflect the current state of the discipline in analysis, experimental observation, and numerical simulation. In the interest of achieving this goal, authors are encouraged to consider the significance of their contributions for the field of mechanics and the implications of their results, in addition to describing the details of their work.