title: Biochemomechanics of cerebral vasospasm and its resolution: II. Constitutive relations and model simulations.
abstract: Cerebral vasospasm is a poorly understood clinical condition that appears to result from complex biochemical and biomechanical processes that manifest as yet another example of vascular growth and remodeling. We submit that mathematical modeling holds great promise to help synthesize diverse types of data and thereby to increase our understanding of vasospasm. Toward this ultimate goal, we present constitutive relations and parametric studies that illustrate the potential utility of a new theoretical framework that combines information on wall mechanics, hemodynamics, and chemical kinetics. In particular, we show that chemical and mechanical mediators of cellular and extracellular matrix turnover can differentially dominate the progression and resolution of vasospasm. Moreover, based on our simulations, endothelial damage can significantly alter the time-course and extent of vasospasm as can impairment of autoregulation. Although the present results are consistent with salient features of clinically reported vasospasm, and thus provide some new insight, we suggest that most importantly they reveal areas of pressing need with regard to the collection of additional experimental data. Without appropriate data, our understanding of cerebral vasospasm will remain incomplete.
authors.affiliation: Department of Mechanical Engineering, Michigan State University, East Lansing, MI, USA.
authors.forename: S
authors.initials: S
authors.lastname: Baek
authors.forename: A
authors.initials: A
authors.lastname: Valentín
authors.forename: J D
authors.initials: JD
authors.lastname: Humphrey
mesh_terms: D001696:Biomechanical Phenomena; D002536:Cerebral Arteries / Q000502:physiology; D002560:Cerebrovascular Circulation / Q000502:physiology; D003198:Computer Simulation; D006801:Humans; D008955:Models, Cardiovascular; D014661:Vasoconstriction / Q000502:physiology; D020301:Vasospasm, Intracranial / Q000209:etiology* / Q000503:physiopathology*