Strain-induced collagen denaturation is rate dependent in failure of cerebral arteries.

While soft tissues are commonly damaged by mechanical loading, the manifestation of this damage at the microstructural level is not fully understood. Specifically, while rate-induced stiffening has been previously observed in cerebral arteries, associated changes in microstructural damage patterns following high-rate loading are largely undefined. In this study, we stretched porcine middle cerebral arteries to failure at 0.

Stretch-Induced Intimal Failure in Isolated Cerebral Arteries as a Function of Development.

Recent clinical studies have shown that traumatic brain injury is a significant risk factor for stroke. Motivated to better understand possible mechanisms of this association, we studied subfailure disruption of the intima in overstretched sheep cerebral arteries, as this has been implicated in the increased risk of stroke following blunt cerebrovascular injury. Middle cerebral arteries from four age groups (ranging from fetal to adult) were stretched axially to failure, and intimal disruption was captured with a video camera.

Biaxial softening of isolated cerebral arteries following axial overstretch.

Arteries play a critical role in carrying essential nutrients and oxygen throughout the brain; however, vessels can become damaged in traumatic brain injury (TBI), putting neural tissue at risk. Even in the absence of hemorrhage, large deformations can disrupt both the physiological and mechanical behavior of the cerebral vessels. Our group recently reported the effect of vessel overstretch on axial mechanics; however, that work did not address possible changes in circumferential mechanics that are critical to the regulation of blood flow.

Molecular-level collagen damage explains softening and failure of arterial tissues: A quantitative interpretation of CHP data with a novel elasto-damage model.

The present experimental-modelling study provides a quantitative interpretation of mechanical data and damage measurements obtained from collagen hybridizing peptide (CHP) techniques on overstretched sheep cerebral arterial tissues. To this aim, a structurally-motivated constitutive model is developed in the framework of continuum damage mechanics. The model includes two internal variables for describing the effects of collagen triple-helical unfolding via interstrand delamination: one governs plastic mechanisms in collagen fibers, leading to a stress softening response of the tissue at the macroscale; the other one describes the loss of fiber structural integrity, leading to tissue final failure.

Cerebral blood vessel damage in traumatic brain injury.

Traumatic brain injury is a devastating cause of death and disability. Although injury of brain tissue is of primary interest in head trauma, nearly all significant cases include damage of the cerebral blood vessels. Because vessels are critical to the maintenance of the healthy brain, any injury or dysfunction of the vasculature puts neural tissue at risk.

Detection and characterization of molecular-level collagen damage in overstretched cerebral arteries.

Unlabelled: It is well established that overstretch of arteries alters their mechanics and compromises their function. However, the underlying structural mechanisms behind these changes are poorly understood. Utilizing a recently developed collagen hybridizing peptide (CHP), we demonstrate that a single mechanical overstretch of an artery produces molecular-level unfolding of collagen.

Development of Mechanical and Failure Properties in Sheep Cerebral Arteries.

Traumatic brain injury (TBI) is a devastating problem for people of all ages, but the nature of the response to such injury is often different in children than in adults. Cerebral vessel damage and dysfunction are common following TBI, but age-dependent, large-deformation vessel response has not been characterized. Our objective was to investigate the mechanical properties of cerebral arteries as a function of development.