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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

Data from a representative sample showing the definitions of (A) the baseline stress from the initial pre-overstretch baseline test (at 1.03*λIV) and (B) the baseline stretch levels λZ1 (from the overstretch test; λZ max = 1.3*λIV) and λZ2 (from the post-overstretch failure test; cropped data shown) corresponding to the baseline stress. (●) indicates the undamaged in vivo stress-stretch state.
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Figure 1: Data from a representative sample showing the definitions of (A) the baseline stress from the initial pre-overstretch baseline test (at 1.03*λIV) and (B) the baseline stretch levels λZ1 (from the overstretch test; λZ max = 1.3*λIV) and λZ2 (from the post-overstretch failure test; cropped data shown) corresponding to the baseline stress. (●) indicates the undamaged in vivo stress-stretch state.

Mentions: To quantify the effect of overstretch, five parameters derived from the pre- and post-damage stress-stretch curves were compared: in vivo stiffness, tare load stretch, baseline stretch, strain energy, and failure values. In vivo stiffness was calculated as the slope of the curve at in vivo stretch in pressurized axial stretch tests (Monson et al., 2008; Bell et al., 2013). Tare load stretch was defined as the stretch value associated with an axial load of 0.0005 N, a force value consistently outside the noise range of the load cell, intended to help identify possible changes in reference length. Additionally, baseline stress was defined as the axial stress level corresponding to 1.03*λIV in the pre-overstretch baseline test (Figure 1A). The corresponding stretch level was defined as the baseline stretch and was quantified in both the overstretch test (λZ1) and the post-overstretch failure test (λZ2) since both always included the baseline stress level (Figure 1B). The initial measurement of baseline stress was taken at 1.03*λIV rather than the maximum applied stretch (1.05*λIV) in order to avoid any artifacts in the data caused by deceleration of the actuator near the peak stretch level. The percent change in axial stretch for both the tare load stretch and the baseline stretch was calculated using (Eq. 6).(6)%Δλz=100∗λ2−λ1λ1where λ1 and λ2 are the relevant pre- and post-damage stretch values. Similar to work by others (Maher et al., 2012b), softening was also quantified using percent change in strain energy (%ΔU) (Eq. 7), where A1 and A2 are the areas under the curve to the overstretch level before and after damage, respectively, except in the case of repeated baseline tests where the maximum stretch was 1.05*λIV.(7)%ΔU=100∗A1−A2A1


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

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

Data from a representative sample showing the definitions of (A) the baseline stress from the initial pre-overstretch baseline test (at 1.03*λIV) and (B) the baseline stretch levels λZ1 (from the overstretch test; λZ max = 1.3*λIV) and λZ2 (from the post-overstretch failure test; cropped data shown) corresponding to the baseline stress. (●) indicates the undamaged in vivo stress-stretch state.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 1: Data from a representative sample showing the definitions of (A) the baseline stress from the initial pre-overstretch baseline test (at 1.03*λIV) and (B) the baseline stretch levels λZ1 (from the overstretch test; λZ max = 1.3*λIV) and λZ2 (from the post-overstretch failure test; cropped data shown) corresponding to the baseline stress. (●) indicates the undamaged in vivo stress-stretch state.
Mentions: To quantify the effect of overstretch, five parameters derived from the pre- and post-damage stress-stretch curves were compared: in vivo stiffness, tare load stretch, baseline stretch, strain energy, and failure values. In vivo stiffness was calculated as the slope of the curve at in vivo stretch in pressurized axial stretch tests (Monson et al., 2008; Bell et al., 2013). Tare load stretch was defined as the stretch value associated with an axial load of 0.0005 N, a force value consistently outside the noise range of the load cell, intended to help identify possible changes in reference length. Additionally, baseline stress was defined as the axial stress level corresponding to 1.03*λIV in the pre-overstretch baseline test (Figure 1A). The corresponding stretch level was defined as the baseline stretch and was quantified in both the overstretch test (λZ1) and the post-overstretch failure test (λZ2) since both always included the baseline stress level (Figure 1B). The initial measurement of baseline stress was taken at 1.03*λIV rather than the maximum applied stretch (1.05*λIV) in order to avoid any artifacts in the data caused by deceleration of the actuator near the peak stretch level. The percent change in axial stretch for both the tare load stretch and the baseline stretch was calculated using (Eq. 6).(6)%Δλz=100∗λ2−λ1λ1where λ1 and λ2 are the relevant pre- and post-damage stretch values. Similar to work by others (Maher et al., 2012b), softening was also quantified using percent change in strain energy (%ΔU) (Eq. 7), where A1 and A2 are the areas under the curve to the overstretch level before and after damage, respectively, except in the case of repeated baseline tests where the maximum stretch was 1.05*λIV.(7)%ΔU=100∗A1−A2A1

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