Damage to the rat cerebrum under in vitro sinusoidal translational shear deformation.

Blast waves, which induce sinusoidal shear waves within brain tissue, may cause mild traumatic brain injury (mTBI). To identify damage from a shear deformation wave, sagittal slices of rat cerebra are subjected to 50 cycles of translational shear deformation at six fixed frequencies between 25 Hz and 125 Hz and displacement amplitudes of 10% or 25% of the original length of the specimen. Each deformation frequency produces transient and apparent steady shear stress states that frequency analysis describes by their harmonic wavelet and Fourier frequency components. The dominant frequency components are integer multiples of the applied deformation frequency. The morphology of the shear stress versus time curve, and probably the type of damage, changes with deformation frequency. Damage at the lower frequencies appears to be diffuse bond breaking. Imaging and histology do not clearly detect mild damage due to bond breaking that underlies mTBI, which the analysis of the shear stress response captures. Major transitions in the morphology of the stress response in the two regions occur at about 75 Hz deformation frequency, possibly due to minor damage to cerebral substructures. An increase in deformation frequency increases the drag force between the extracellular fluid and solid matter. The deformation frequency dependence of the shear stress response makes protection against blast mTBI more difficult because the frequency content of a blast wave is not known a priori.

Interstitial fluid-solid interaction within aneurysmal and non-pathological human ascending aortic tissue under translational sinusoidal shear deformation.

The interaction shear force between internal interstitial fluid motion and the solid circumferential-longitudinal medial lamellae helps generate the shear stress involved in dissection of human ascending aorta aneurysmal or non-pathologic tissue. Frequency analysis parameters from the total shear stress versus time response to translational 1 Hz sinusoidal shear deformation over 50 cycles measure the interaction with respect to the three factors: tissue type, sinusoidal deformation amplitude and direction of the shear deformation. Significant 1, 3, and 5 Hz components exist in this order of descending magnitude for shear deformation amplitudes of either 25% or 50% of the specimen length. Evaporation tests indicate that the amount of free water in both aneurysmal and non-pathological tissue is nearly the same. The interstitial fluid-solid interaction under shear deformation is visible in the shoulders of the total shear stress versus time response curve that are caused by the 3 Hz component. During a single deformation cycle, the ratio of the amplitudes of the 3 Hz and the 1 Hz components measures the normalized amount of interaction. Under translational sinusoidal shear deformation at 25% amplitude, this interaction ratio is statistically smaller in non-pathologic than in aneurysmal human ascending aortic tissue in the circumferential direction. The frequency analysis parameters provide evidence that the structural changes in aneurysmal tissue induce an increase in the interstitial fluid-medial solid interaction shear force which contributes to the propensity for aneurysmal rupture. STATEMENT OF SIGNIFICANCE: Circumferential shear force between the interstitial fluid and medial lamellae within the human ascending aortic wall is demonstrably greater in aneurysmal than non-pathologic tissue. This force likely increases with medial elastin degeneration and may facilitate the dissection propensity in aneurysmal tissue. The 3 Hz component in frequency analyses of the total shear stress versus time curve produced by 1 Hz sinusoidal translational shear deformation measures the fluid-solid interaction shear force that is otherwise difficult to isolate. This non-standard examination of the interstitial fluid interaction helps clarify clinical mechanical implications of structural differences between aneurysmal and non-pathologic human ascending aortic tissue. The aneurysmal dissection susceptibility does not appear to depend on the amount of interstitial fluid or the wall thickness compared to non-pathologic tissue.

Comparison of aneurysmal and non-pathologic human ascending aortic tissue in shear.

BACKGROUND: The mechanical properties of the aorta may provide some guidance to cardiovascular surgeons treating aortic disease. While tensile tests are traditional, recent work suggests that shear is important in aortic dissection. Characterizing the differences or similarities in the mechanical shear stress response of non-pathologic human ascending aortic tissue and of tissue that has remodeled to become aneurysmal contributes to understanding the differences in behavior of the two tissues. METHODS: Fresh non-pathological and aneurysmal tissue acquired from the operating room is deformed in translational shear at approximately physiological rates to 67% deformation followed by stress relaxation to allow comparison of their mechanical behavior. Aneurysmal tissue is tested at 1 mm/s or 12 mm/s and normal tissue at 12 mm/s. The deformation is either in the circumferential or longitudinal direction for a total of 48 specimens. FINDINGS: The shear response at 12 mm/s in non-pathological and aneurysmal tissue is similar in the circumferential direction but different in the longitudinal direction. Tissue type accounts for up to 30% of the variation in the longitudinal direction. The aneurysmal tissue response is rate-dependent. Both tissues exhibit significant shear stress relaxation. INTERPRETATION: Remodeling to create the aneurysm modifies the bond strength between collagen fibers and the extracellular matrix. The time-dependent response is probably due to interstitial fluid behavior. Thoracic surgeons must use caution in applying aortic stress values in the literature because they depend on the deformation rate.

Influence of high deformation rate, brain region, transverse compression, and specimen size on rat brain shear stress morphology and magnitude.

An external mechanical insult to the brain, such as a blast, may create internal stress and deformation waves, which have shear and longitudinal components that can induce combined shear and compression of the brain tissue. To isolate the consequences of such interactions for the shear stress and to investigate the role of the extracellular fluid in the mechanical response, translational shear stretch at 10/s, 60/s, and 100/s translational shear rates under either 0% or 33% fixed transverse compression is applied without preconditioning to rat brain specimens. The specimens from the cerebrum, the cerebellum grey matter, and the brainstem white matter are nearly the full length of their respective regions. The translational shear stress response to translational shear deformation is characterized by the effect that each of four factors, high deformation rate, brain region, transverse compression, and specimen size, have on the shear stress magnitude averaged over ten specimens for each combination of factors. Increasing the deformation rate increases the magnitude of the shear stress at a given translational shear stretch, and as tested by ANOVAs so does applying transverse fixed compression of 33% of the thickness. The stress magnitude differs by the region that is the specimen source: cerebrum, cerebellum or brainstem. The magnitude of the shear stress response at a given deformation rate and stretch depends on the specimen length, called a specimen size effect. Surprisingly, under no compression a shorter length specimen requires more shear stress, but under 33% compression a shorter length specimen requires less shear stress, to meet a required shear deformation rate. The shear specimen size effect calls into question the applicability of the classical shear stress definition to hydrated soft biological tissue.