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Subfailure overstretch induces persistent changes in the passive mechanical response of cerebral arteries.

Bell ED, Sullivan JW, Monson KL - Front Bioeng Biotechnol (2015)

Bottom Line: This subfailure deformation could result in altered mechanical behavior.The observed softening also generally resulted in increased non-linearity of the stress-stretch curve, with toe region slope decreasing and large deformation slope increasing.These changes may have significant implications in repeated TBI events and in increased susceptibility to stroke post-TBI.

View Article: PubMed Central - PubMed

Affiliation: Department of Bioengineering, University of Utah , Salt Lake City, UT , USA ; Laboratory of Head Injury and Vessel Biomechanics, Department of Mechanical Engineering, University of Utah , Salt Lake City, UT , USA.

ABSTRACT
Cerebral blood vessels are critical in maintaining the health of the brain, but their function can be disrupted by traumatic brain injury (TBI). Even in cases without hemorrhage, vessels are deformed with the surrounding brain tissue. This subfailure deformation could result in altered mechanical behavior. This study investigates the effect of overstretch on the passive behavior of isolated middle cerebral arteries (MCAs), with the hypothesis that axial stretch beyond the in vivo length alters this response. Twenty nine MCA sections from 11 ewes were tested. Vessels were subjected to a baseline test consisting of an axial stretch from a buckled state to 1.05* in vivo stretch (λIV) while pressurized at 13.3 kPa. Specimens were then subjected to a target level of axial overstretch between 1.05*λIV (λz = 1.15) and 1.52*λIV (λz = 1.63). Following overstretch, baseline tests were repeated immediately and then every 10 min, for 60 min, to investigate viscoelastic recovery. Injury was defined as an unrecoverable change in the passive mechanical response following overstretch. Finally, pressurized MCAs were pulled axially to failure. Post-overstretch response exhibited softening such that stress values at a given level of stretch were lower after injury. The observed softening also generally resulted in increased non-linearity of the stress-stretch curve, with toe region slope decreasing and large deformation slope increasing. There was no detectable change in reference configuration or failure values. As hypothesized, the magnitude of these alterations increased with overstretch severity, but only once overstretch exceeded 1.2*λIV (p < 0.001). These changes were persistent over 60 min. These changes may have significant implications in repeated TBI events and in increased susceptibility to stroke post-TBI.

No MeSH data available.


Related in: MedlinePlus

Percent decrease in axial in vivo stiffness following overstretch. Red error bars indicate SD for each group. Blue line connects group means to clarify trends. (○) indicates individual data points. (*) indicates statistical difference from pre-overstretch values. (#) indicates statistical difference from the group subjected to an overstretch two levels lower.
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Figure 3: Percent decrease in axial in vivo stiffness following overstretch. Red error bars indicate SD for each group. Blue line connects group means to clarify trends. (○) indicates individual data points. (*) indicates statistical difference from pre-overstretch values. (#) indicates statistical difference from the group subjected to an overstretch two levels lower.

Mentions: In vivo axial stiffness was shown to decrease with overstretch (Figure 3). However, this change in stiffness was non-linear, with less difference between adjacent groups with higher overstretch. Mean pre-overstretch in vivo stiffness was 0.65 (±0.13) MPa. In vivo stiffnesses from the control (non-overstretched) and 1.1*λIV overstretch groups were not significantly different from the pre-damage value (Table 1). However, the measure was significantly reduced following each of the higher overstretch levels, with reductions of 40 and 80% following overstretches of 1.2 and 1.5, respectively. None of the large overstretch groups was found to be different from the adjacent group at a lower stretch level. However, the 1.3*λIV (p < 0.001) and 1.4*λIV (p = 0.0058) groups were statistically different from the overstretch group two levels lower. The 1.5*λIV group was not significantly different from the 1.3*λIV group (p = 0.16).


Subfailure overstretch induces persistent changes in the passive mechanical response of cerebral arteries.

Bell ED, Sullivan JW, Monson KL - Front Bioeng Biotechnol (2015)

Percent decrease in axial in vivo stiffness following overstretch. Red error bars indicate SD for each group. Blue line connects group means to clarify trends. (○) indicates individual data points. (*) indicates statistical difference from pre-overstretch values. (#) indicates statistical difference from the group subjected to an overstretch two levels lower.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4309201&req=5

Figure 3: Percent decrease in axial in vivo stiffness following overstretch. Red error bars indicate SD for each group. Blue line connects group means to clarify trends. (○) indicates individual data points. (*) indicates statistical difference from pre-overstretch values. (#) indicates statistical difference from the group subjected to an overstretch two levels lower.
Mentions: In vivo axial stiffness was shown to decrease with overstretch (Figure 3). However, this change in stiffness was non-linear, with less difference between adjacent groups with higher overstretch. Mean pre-overstretch in vivo stiffness was 0.65 (±0.13) MPa. In vivo stiffnesses from the control (non-overstretched) and 1.1*λIV overstretch groups were not significantly different from the pre-damage value (Table 1). However, the measure was significantly reduced following each of the higher overstretch levels, with reductions of 40 and 80% following overstretches of 1.2 and 1.5, respectively. None of the large overstretch groups was found to be different from the adjacent group at a lower stretch level. However, the 1.3*λIV (p < 0.001) and 1.4*λIV (p = 0.0058) groups were statistically different from the overstretch group two levels lower. The 1.5*λIV group was not significantly different from the 1.3*λIV group (p = 0.16).

Bottom Line: This subfailure deformation could result in altered mechanical behavior.The observed softening also generally resulted in increased non-linearity of the stress-stretch curve, with toe region slope decreasing and large deformation slope increasing.These changes may have significant implications in repeated TBI events and in increased susceptibility to stroke post-TBI.

View Article: PubMed Central - PubMed

Affiliation: Department of Bioengineering, University of Utah , Salt Lake City, UT , USA ; Laboratory of Head Injury and Vessel Biomechanics, Department of Mechanical Engineering, University of Utah , Salt Lake City, UT , USA.

ABSTRACT
Cerebral blood vessels are critical in maintaining the health of the brain, but their function can be disrupted by traumatic brain injury (TBI). Even in cases without hemorrhage, vessels are deformed with the surrounding brain tissue. This subfailure deformation could result in altered mechanical behavior. This study investigates the effect of overstretch on the passive behavior of isolated middle cerebral arteries (MCAs), with the hypothesis that axial stretch beyond the in vivo length alters this response. Twenty nine MCA sections from 11 ewes were tested. Vessels were subjected to a baseline test consisting of an axial stretch from a buckled state to 1.05* in vivo stretch (λIV) while pressurized at 13.3 kPa. Specimens were then subjected to a target level of axial overstretch between 1.05*λIV (λz = 1.15) and 1.52*λIV (λz = 1.63). Following overstretch, baseline tests were repeated immediately and then every 10 min, for 60 min, to investigate viscoelastic recovery. Injury was defined as an unrecoverable change in the passive mechanical response following overstretch. Finally, pressurized MCAs were pulled axially to failure. Post-overstretch response exhibited softening such that stress values at a given level of stretch were lower after injury. The observed softening also generally resulted in increased non-linearity of the stress-stretch curve, with toe region slope decreasing and large deformation slope increasing. There was no detectable change in reference configuration or failure values. As hypothesized, the magnitude of these alterations increased with overstretch severity, but only once overstretch exceeded 1.2*λIV (p < 0.001). These changes were persistent over 60 min. These changes may have significant implications in repeated TBI events and in increased susceptibility to stroke post-TBI.

No MeSH data available.


Related in: MedlinePlus