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Failure and Fatigue Properties of Immature Human and Porcine Parasagittal Bridging Veins.

ABSTRACT: Tearing of the parasagittal bridging veins (BVs) is thought to be a source of extra-axial hemorrhage (EAH) associated with abusive traumatic brain injuries (TBIs) in children. However, the pediatric BV mechanical properties are unknown. We subjected porcine adult, porcine newborn, and human infant BVs to either a low rate pull to failure, a high rate pull to failure, or 30 s of cyclic loading followed by a pull to failure. An additional subset of human infant BVs was examined for viscoelastic recovery between two cycling episodes. We found that human infant BVs are stronger than porcine BVs, and BV mechanical properties are rate dependent, but not age dependent. Successive cyclic loading to a uniform level of stretch softened BVs with decaying peak stresses, and shifted their stress-stretch relationship. These data are critical in understanding BV tissue behavior in accidental and abusive trauma scenarios, which in turn may clarify circumstances that may be injurious to young children.

SUBMITTER: Pasquesi SA

PROVIDER: S-EPMC5529232 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature

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Failure and Fatigue Properties of Immature Human and Porcine Parasagittal Bridging Veins.

Pasquesi Stephanie A SA Margulies Susan S SS

Annals of biomedical engineering 20170412 8

Tearing of the parasagittal bridging veins (BVs) is thought to be a source of extra-axial hemorrhage (EAH) associated with abusive traumatic brain injuries (TBIs) in children. However, the pediatric BV mechanical properties are unknown. We subjected porcine adult, porcine newborn, and human infant BVs to either a low rate pull to failure, a high rate pull to failure, or 30 s of cyclic loading followed by a pull to failure. An additional subset of human infant BVs was examined for viscoelastic re ...[more]

PMID: 28405773

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Project description:KEY POINTS:As reactivation of the fetal gene program has been implicated in pathological remodelling during heart failure (HF), we examined whether cardiomyocyte subcellular structure and function revert to an immature phenotype during this disease. Surface and internal membrane structures appeared gradually during development, and returned to a juvenile state during HF. Similarly, dyadic junctions between the cell membrane and sarcoplasmic reticulum were progressively 'packed' with L-type Ca2+ channels and ryanodine receptors during development, and 'unpacked' during HF. Despite similarities in subcellular structure, dyads were observed to be functional from early developmental stages, but exhibited an impaired ability to release Ca2+ in failing cardiomyocytes. Thus, while immature and failing cardiomyocytes share similarities in subcellular structure, these do not fully account for the marked impairment of Ca2+ homeostasis observed in HF. ABSTRACT:Reactivation of the fetal gene programme has been implicated as a driver of pathological cardiac remodelling. Here we examined whether pathological remodelling of cardiomyocyte substructure and function during heart failure (HF) reflects a reversion to an immature phenotype. Using scanning electron microscopy, we observed that Z-grooves and t-tubule openings at the cell surface appeared gradually during cardiac development, and disappeared during HF. Confocal and super-resolution imaging within the cell interior revealed similar structural parallels; disorganization of t-tubules in failing cells was strikingly reminiscent of the late stages of postnatal development, with fewer transverse elements and a high proportion of longitudinal tubules. Ryanodine receptors (RyRs) were observed to be laid down in advance of developing t-tubules and similarly 'orphaned' in HF, although RyR distribution along Z-lines was relatively sparse. Indeed, nanoscale imaging revealed coordinated packing of L-type Ca2+ channels and RyRs into dyadic junctions during development, and orderly unpacking during HF. These findings support a 'last in, first out' paradigm, as the latest stages of dyadic structural development are reversed during disease. Paired imaging of t-tubules and Ca2+ showed that the disorganized arrangement of dyads in immature and failing cells promoted desynchronized and slowed Ca2+ release in these two states. However, while developing cells exhibited efficient triggering of Ca2+ release at newly formed dyads, dyadic function was impaired in failing cells despite similar organization of Ca2+ handling proteins. Thus, pathologically deficient Ca2+ homeostasis during HF is only partly linked to the re-emergence of immature subcellular structure, and additionally reflects lost dyadic functionality.

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Dataset Information

Failure and Fatigue Properties of Immature Human and Porcine Parasagittal Bridging Veins.

Publications

Failure and Fatigue Properties of Immature Human and Porcine Parasagittal Bridging Veins.

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