A cerebral blood flow increase of 36 ± 15% sounds like it could be very important immediately post stroke! It's been almost 4 years, has ANYTHING AT ALL been done in the stroke world on this? Or do we have fucking failures of stroke associations doing nothing once again?
No clue, so ask your doctor what this means.
Viscoelasticity is defined as the time-dependent response of a material subjected to a constant load or deformation (Cohen, Foster, & Mow, 1998). From: Human Orthopaedic Biomechanics, 2022.
What is Hypercapnia?
Hypercapnia increases brain viscoelasticity
Abstract
Brain function, the brain’s metabolic activity, cerebral blood flow (CBF), and intracranial pressure are intimately linked within the tightly autoregulated regime of intracranial physiology in which the role of tissue viscoelasticity remains elusive. We applied multifrequency magnetic resonance elastography (MRE) paired with CBF measurements in 14 healthy subjects exposed to 5-min carbon dioxide-enriched breathing air to induce cerebral vasodilatation by hypercapnia. Stiffness and viscosity as quantified by the magnitude and phase angle of the complex shear modulus, |G*| and ϕ, as well as CBF of the whole brain and 25 gray matter sub-regions were analyzed prior to, during, and after hypercapnia. In all subjects, whole-brain stiffness and viscosity increased due to hypercapnia by 3.3 ± 1.9% and 2.0 ± 1.1% which was accompanied by a CBF increase of 36 ± 15%. Post-hypercapnia, |G*| and ϕ reduced to normal values while CBF decreased by 13 ± 15% below baseline. Hypercapnia-induced viscosity changes correlated with CBF changes, whereas stiffness changes did not. The MRE-measured viscosity changes correlated with blood viscosity changes predicted by the Fåhræus–Lindqvist model and microvessel diameter changes from the literature. Our results suggest that brain viscoelastic properties are influenced by microvessel blood flow and blood viscosity: vasodilatation and increased blood viscosity due to hypercapnia result in an increase in MRE values related to viscosity.
Results
Figure 3 shows group-averaged perfusion and stiffness maps of one representative image slice for the three phases of the hypercapnia challenge. Figure 4 shows the group-averaged values of whole-brain perfusion, stiffness, and viscosity next to the average values of BP and HR. All of them follow a similar pattern: (i) highly significant increase from normocapnia to hypercapnia: Δ|G*| = +3.3 ± 1.9% (p = 1.1 × 10−5), Δϕ = +2.0 ± 1.1% (p = 1.8 × 10−6), ΔCBF = + 36 ± 15% (p = 1.7 × 10−7), ΔBP = +3.4 ± 3.0% (p = 4.3 × 10−3), ΔHR = +5.1 ± 6.0% (p = 5.2 × 10−3); (ii) decrease after hypercapnia with significant differences for stiffness, viscosity, and perfusion only: Δ|G*| = −2.4 ± 1.9% (p = 3.9 × 10−4), ΔBP = −0.8 ± 3.7% (p = 4.5 × 10−1), Δϕ = −2.0 ± 0.7% (p = 1.2 × 10−6), ΔHR = −2.3 ± 6.4% (p = 9.6 × 10−2), and ΔCBF = −36 ± 11% (p = 1.6 × 10−7). For an overview of all group-averaged whole-brain MRE and CBF values, see Table 1.
Group-averaged perfusion, stiffness, and viscosity maps of one exemplary slice in Montreal Neurological Institute space for the three phases of the hypercapnia challenge. See Figure 2(b) for the corresponding map of analyzed AAL atlas regions in the same slice. Note the pronounced CBF offset in the auditory cortex activated by the scanner noise (Heschl’s gyrus—ROI #23, white arrow). CBF: cerebral blood flow.
Highly significant increase in all parameters between normocapnia and hypercapnia (red). Decrease in all measured parameters after hypercapnia (blue) with significant differences for whole-brain perfusion, stiffness, and viscosity only (*p < 0.05; **p < 0.01; ***p < 0.001). Note the significant CBF drop under baseline (dashed line) after hypercapnia. For detailed values, see Table 1. CBF: cerebral blood flow.
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