Pith. sign in

REVIEW 4 major objections 5 minor 36 references

Coupled Modeling of External Pressure and Capillary Blood Flow: Nonlinear Dynamics of Vascular Elasticity and Collapse Effects

T0 review · 4 major / 5 minor · reviewed 2026-08-06 · deepseek-v4-flash

Challenge this review Re-run · record.json Download PDF Read on arXiv ↗ Review JSON

Pith's one-line read This paper proposes that capillary blood flow under external pressure follows a three-branch law: elastic compression below 30 mmHg, elliptical collapse from 30 to 40 mmHg, and exponential decay above 40 mmHg.

desk verdict The three-branch formula is internally inconsistent under the paper's own baseline parameters: the elastic branch closes the vessel at 7.5 mmHg and the high-pressure branch jumps upward at 40 mmHg, so the central dose-response law as written is not a valid model. read the letter →

arxiv 2507.13653 v1 pith:KNA6WIE3 submitted 2025-07-18 physics.bio-ph physics.med-ph

Xinyi Cai , Hanyue Mo , Yuyao Chang , Kun Cheng This is my paper · ORCID
classification physics.bio-phphysics.med-ph
keywords capillarybloodflowexternalpressurevascularcollapsethree-phasemodelhemodynamicsmicrocirculationtherapydose-response
verification ladder T0 review T1 audit T2 compute T3 formal

The pith

A machine-rendered reading of the paper's core claim, the machinery that carries it, and where it could break.

The reading

This paper proposes a quantitative, piecewise law for how external pressure reduces capillary blood flow. It claims that the pressure–flow curve splits into three regimes: elastic compression below 30 mmHg, elliptical collapse between 30 and 40 mmHg, and exponential decay above 40 mmHg, each with an explicit formula. The payoff is a dose–response tool for pressure-based treatments such as tourniquets and compression garments, with patient-specific parameters for vessel stiffness, collapse threshold, and decay rate. The paper argues that the model captures the key determinants and matches literature trends in each pressure range.

What carries the argument

The argument rides on a piecewise application of Poiseuille's law, $Q \propto R^4$, where the effective radius $R(q)$ is replaced by three deformation laws. In the low-pressure branch, $R = r_0(1 - q r_0/(E h))$ from linear elasticity; in the transition branch, the quartic collapse factor $(1 - q/K_{\text{collapse}})^4$ is multiplied by an elliptical resistance correction $\beta = (a/b)^2/(1 + (a/b)^2)$; in the high-pressure branch, the lumen closure is modeled as an exponential decay $\exp(-\alpha(q-40))$. These three mechanisms carry the entire modeling claim: there is no other fitting or computational machinery in the paper beyond these algebraic expressions and the sensitivity scans around them.

What would settle it

Measure capillary flow under external pressure from 0 to 60 mmHg in a vessel with the Table 1 parameters. The model's first branch predicts $Q=0$ at $q = Eh/r_0 \approx 7.5$ mmHg; observing measurable flow at, say, 20 mmHg, or a decline that is not quartic, would refute the first branch and with it the three-phase curve.

Watch

Extended reading notes

Core claim

On the paper's own terms, the central result is Eq. (2): normalized flow $Q(q)/Q_0$ equals $(1 - q r_0/(E h))^4$ for $q < 30$ mmHg, $(1 - q/K_{ ext{collapse}})^4 \beta(q)$ for $30 \leq q < 40$ mmHg, and $\exp(-\alpha(q-40))$ for $q \geq 40$ mmHg. Here $Q_0$ is the undisturbed flow, $r_0$ the initial radius, $E$ the wall elastic modulus, $h$ the wall thickness, $K_{\text{collapse}}$ a stiffness parameter, $\beta$ a function of the elliptical aspect ratio, and $\alpha$ a decay coefficient. The three branches are claimed to correspond to distinct physical deformation mechanisms: linear elastic compression, shell-buckling into an ellipse, and lumen closure. The paper presents sensitivity analyses and literature comparisons as evidence that this three-phase structure describes capillary flow under external pressure.

Load-bearing premise

The three-phase law rests on the premise that, below 30 mmHg, the capillary radius shrinks linearly as $R(q)=r_0(1 - q r_0/(E h))$; with the paper's own baseline values ($E=10$ kPa, $r_0=0.01$ mm, $h=0.001$ mm), this radius reaches zero at about 7.5 mmHg, well inside the claimed elastic phase.

Editorial extensions

If this is right

  • Below 30 mmHg, the model predicts that flow is governed by the quartic of a linearly compressed radius, so higher elastic modulus $E$ or thicker wall $h$ preserves perfusion under the same pressure.
  • In the 30–40 mmHg band, flow drops steeply and the reduction is controlled jointly by the collapse stiffness $K$ and the elliptical aspect-ratio factor $\beta$, so vessels that are already elliptical (fibrosis, edema) lose perfusion faster.
  • Above 40 mmHg, flow decays exponentially with rate $\alpha$, meaning residual perfusion at high pressure is set by $\alpha$ and not by wall elasticity.
  • The piecewise structure implies a safety threshold: compression therapy should stay below roughly 30–40 mmHg to avoid collapse, and brief excursions above 40 mmHg could be used deliberately for hemostasis.
  • Because $E$, $K$, $\beta$, and $\alpha$ are patient-specific, the model yields an individual pressure–flow dose–response curve for tourniquets and compression garments.

Reading between the lines

Editorial extensions of the paper, not claims the author makes directly.

  • From the paper's own baseline parameters, the elastic branch reaches zero flow at $q = Eh/r_0 \approx 7.5$ mmHg, far below the claimed 30 mmHg boundary; if this linear-compression law is taken literally, the first branch must be replaced by a nonlinear elasticity before the three-phase picture can be upheld. This is an inference about internal consistency, not a paper claim.
  • The threshold structure suggests a direct experiment: if 30 and 40 mmHg are real physiological boundaries, compression garments below 30 mmHg should preserve perfusion while those above 40 mmHg should show a sharp exponential ischemia; laser speckle contrast imaging or OCT could test this without new modeling.
  • Applying the elastic branch to suction by substituting $q \rightarrow -q$ predicts flow enhancement at moderate negative pressure; the paper only notes a tentative link to existing observations, so this is a testable extension, not a paper claim.
  • The transition branch uses $\beta$ as a fitted constant; a full shell-buckling model that computes the aspect ratio $a/b$ from the applied pressure would remove that fit and make the branch fully predictive.
Share X Bluesky LinkedIn Reddit HN

Signed reviews

No signed human review yet.

Editorial analysis

A structured set of objections, weighed in public.

Desk editor's note, referee report, and a circularity audit.

Referee Report

4 major / 5 minor

Summary. The paper proposes a three-phase piecewise model for capillary blood flow under external pressure: an elastic-compression regime for q < 30 mmHg, an elliptical-collapse transition for 30 ≤ q < 40 mmHg, and an exponential closure-decay regime for q ≥ 40 mmHg. The central quantitative claim is Eq. (2), which expresses normalized flow Q(q)/Q0 as (1 − q r0/(E h))^4, (1 − q/K_collapse)^4·β(q), and exp(−α(q−40)) in the three regimes. The authors perform sensitivity analyses for the parameters E, K, and α, present simulated error-bar analyses, and compare qualitative trends with published literature to argue that the model captures key determinants of pressure-induced flow reduction and can support dose–response assessment for compression therapies.

Significance. If the model were quantitatively valid, it would provide a closed-form, parameterized tool for predicting capillary perfusion under external pressure, with potential utility in tourniquet and compression-garment dosing and patient-specific tuning. The paper is also explicit about its mechanistic assumptions and provides sensitivity maps that could guide future experiments. However, the central law Eq. (2) is internally inconsistent under the paper's own default parameters: the low-pressure branch becomes unphysical at 7.5 mmHg, predicting growing flow instead of attenuation throughout most of the claimed 0–30 mmHg elastic phase, and the piecewise function has a large upward discontinuity at the 40 mmHg boundary. These are load-bearing arithmetic defects, not merely presentation issues. The validation is also circular because the error bars are generated from the model's own simulated outputs and then used to assert reliability, and the literature comparison is qualitative rather than a test of the specific functional forms. The conceptual three-phase framing may have heuristic value, but the quantitative claim as stated cannot be accepted.

major comments (4)
  1. [§3.2, Eq. (2), first branch] With the paper's own Table 1 defaults (E = 10 kPa, r0 = 0.01 mm, h = 0.001 mm) and 1 mmHg ≈ 133 Pa, the compression term q r0/(E h) equals 1 at q ≈ 7.5 mmHg, so the modeled radius R(q) = r0(1 − q r0/(E h)) reaches zero and then becomes negative inside the claimed 0–30 mmHg elastic phase. For q > 7.5 mmHg the fourth power grows without bound; at q = 30 mmHg the branch would give Q/Q0 = (1 − 30·133·10^−5/(10^4·10^−6))^4 = 81, an increasing flow rather than the monotone attenuation the phase description requires. This contradicts the small-strain (<15%) premise of §2.1 and the statement in §6 that the term only 'approach[es] zero prematurely' for 'certain parameter combinations'; the baseline parameters are exactly one such combination.
  2. [§3.4–§3.5, Eq. (2), boundary at q = 40 mmHg] The piecewise function is discontinuous in the wrong direction at q = 40 mmHg. Approaching from below with the transition-region form and the default values K_collapse = 50 mmHg and β = 0.4 gives Q/Q0 = (1 − 40/50)^4 · 0.4 = 0.00064, while the high-pressure branch at q = 40 gives exp(0) = 1. The flow would thus jump upward by a factor of about 1500 at the moment the vessel supposedly enters the 'closure-induced attenuation' phase, which is inconsistent with the model's own physiological narrative and with the simulated curves in Figures 1–2 that show a continuous decline across this boundary.
  3. [§4, Fig. 2(b,d,f)] The error-bar analysis is circular as a validation. The text states that the data are 'simulated data' used to illustrate model prediction variability; the error bars therefore quantify only the sampling variability of the model's own outputs (with n = 20) and cannot support the conclusions that the model has 'good repeatability,' 'high credibility,' or 'reliability' in the respective pressure regimes. Claims of agreement with physiology would require comparison against independent experimental measurements, which are not provided in the paper.
  4. [§5, literature validation] Section 5 offers only qualitative comparisons with selected references, and several of those studies concern negative pressure, pathological states, or pressure ulcer formation rather than the positive-pressure 0–60 mmHg range of the model. Given that the model contains multiple free parameters (K_collapse, β, α, q_yield, and the 30 and 40 mmHg thresholds), a qualitative match to such trends does not test the specific functional forms in Eq. (2), so the claim that the model is 'validated' is overstated.
minor comments (5)
  1. [§3.2] The endothelial-yield modification Q(q) = Q0(1 − q/q_yield)^4 is introduced in the text but does not appear in the model summary Eq. (2); the relation between this alternative form and the primary low-pressure branch should be made explicit.
  2. [Table 1] β is listed as a 'fitted value' and α as an 'assumption,' but no fitting procedure or data source for these values is described; the reader cannot reproduce the parameter choices.
  3. [Fig. 2(b)] The x-axis labels in panel (b) appear corrupted (e.g., '258.404932449.5868723372.1805583790.90053'), and in the text 'Figure a' should be 'Figure 2(a)'.
  4. [§2.2] The equation for internal pressure P_int = (E h / r0)(r/r0 − 1) is dimensionally inconsistent as written unless the factor (1 − ν^2) is moved to the denominator; please clarify the notation and assumptions for Poisson's ratio.
  5. [References] The reference to Tagliabue (2023) appears incomplete, and several in-text citations (e.g., 'Panula 2022', 'Negosanti et al. 2012') do not follow a consistent format; a careful reference cleanup is needed.

Circularity Check

0 steps flagged · score 0.0 of 10

No circular derivation: Eq. (2) is an explicit piecewise ansatz whose parameters are inputs; the low-pressure closure inconsistency is a physical-validity problem, not circularity.

full rationale

The three-branch law in Eq. (2) is not obtained by fitting a parameter to a subset of data and then predicting a closely related quantity, and it does not rest on a self-citation chain. The low-pressure branch follows algebraically from the explicitly stated linear compression assumption R(q)=r0(1−qr0/(Eh)); the transition branch is an assumed elliptical-correction form with beta and K as inputs; the high-pressure branch is an assumed exponential decay with alpha as an input. None of these inputs is defined in terms of the target flow Q(q) in a way that makes the law tautological after algebraic substitution. The 'fitted value' beta in Table 1 is an uncalibrated input rather than a parameter fitted to a data subset and then used to predict a closely related quantity, so no fitted-input-called-prediction step is exhibited. Section 5's literature comparison is qualitative, and Section 4's error bars are generated from simulated model output, so these are weak validation evidence but not circular derivation. The paper itself flags the low-pressure limitation ('may cause the flow term ... to approach zero prematurely') and the lack of direct clinical validation of the 30/40 mmHg thresholds; these are correctness and evidence concerns, not circularity. No load-bearing citation is authored by the present paper's authors, and no uniqueness theorem is imported. Under the hard rule requiring a specific reduction of a prediction to its inputs, no circular step can be exhibited.

Assumptions & free parameters 6 free parameters · 7 assumptions · 0 invented entities

The model rests on five fitted or assumed numbers (K_collapse, beta, alpha, qyield, and the 30/40 mmHg phase boundaries) and on several imported physical premises: Poiseuille flow driven by a transmural pressure difference, linear thin-wall elasticity, an elliptical resistance factor with no a/b(pressure) law, Han's shell-buckling theory applied to capillaries, and a postulated exponential closure. The paper discloses most of these as assumptions or limitations, which is to its credit, but the disclosure does not reduce their load-bearing role. No new physical entities are introduced.

free parameters (6)
  • K_collapse (critical stiffness) = 50 mmHg
    Listed in Table 1 as 'assumption'. Governs how fast flow falls in the 30-40 mmHg transition branch; no fitting data or physiological measurement is given.
  • beta (elliptical correction) = 0.4
    Table 1 labels beta as a 'fitted value' with no data source. The text defines beta(q) = (a/b)^2/(1+(a/b)^2), but no a/b(q) relation is provided, so beta functions as a hand-chosen constant in every calculation.
  • alpha (closure decay coefficient) = 0.1
    Table 1 labels alpha as 'assumption'. Eq (1) says it 'should be determined based on experimental or physiological data', but no data are used; the high-pressure prediction is entirely determined by this choice.
  • qyield (endothelial yield threshold) = 20 mmHg (example)
    Introduced in Section 3.2 and Discussion as an active-regulation threshold; the value is given as an example ('e.g., 20 mmHg') with no supporting measurement.
  • Phase boundaries at 30 and 40 mmHg = 30 mmHg, 40 mmHg
    Chosen to separate the three phases; Section 5 admits the thresholds 'currently lack direct clinical validation'. The sharp boundaries also create discontinuities between branches.
  • Error-bar simulation protocol = unspecified
    Fig 2(b,d,f) are generated from 'simulated data ... n = 20' with no noise distribution specified, so the claimed SEM values are not reproducible.
assumptions (7)
  • domain assumption Poiseuille's law with a transmural pressure gradient: Delta P is taken as the inside-outside pressure difference and flow variation is wholly attributed to R(q)^4 deformation.
    Section 3.1 uses 'the pressure difference between the inside and outside of the vessel' as the Poiseuille driver while Pint is 'approximately constant'. In reality Poiseuille flow is driven by a longitudinal pressure gradient, not transmural pressure; this conflation is load-bearing for the Q(q) scaling.
  • domain assumption Capillary behaves as a linear-elastic thin-walled tube with small strain, R(q) = r0 (1 - q r0/(E h)).
    Section 3.2 invokes linear elasticity for strains below 15 percent, but with Table 1 values the compression ratio hits 1 at 7.5 mmHg, so the strain exceeds the linear range inside the low-pressure domain.
  • domain assumption Elliptical-tube resistance correction beta(q) = (a/b)^2/(1+(a/b)^2) from Garg et al. applies with no explicit a/b(q) law.
    Sections 2.3 and 3.3 import the factor from the cited literature, but no geometric evolution equation ties a/b to q; in computations beta is a fixed constant (0.4).
  • domain assumption Han's elastic shell buckling theory for sandwich cylindrical shells transfers to capillary cross-section collapse.
    Section 3.3 cites (Han et al. 2004) for the elliptical shape during collapse; that paper treats long sandwich cylindrical shells under external pressure, an extrapolation to single-layer endothelial capillaries with no justification.
  • ad hoc to paper Closure phase flow decays as Q0 exp(-alpha (q-40)).
    Eq (1) in Section 3.4 postulates exponential decay with no derivation; alpha is assumed and the 40 mmHg origin is chosen to match the phase boundary.
  • domain assumption Blood is treated as Newtonian with constant apparent viscosity.
    Sections 2.3 and Discussion acknowledge shear-thinning, cell-free layer, and Fahraeus-Lindqvist effects and defer them to future work; the model uses a single apparent viscosity.
  • standard math Low Reynolds number Stokes flow assumptions apply (Re about 1e-4).
    Section 2.1 cites established microcirculatory rheology; this premise is standard and reasonable for capillaries.

how reviews work

0 comments
Cite this review

Pith. "Pith review of Coupled Modeling of External Pressure and Capillary Blood Flow: Nonlinear Dynamics of Vascular Elasticity and Collapse Effects." pith.science (2026). https://pith.science/paper/KNA6WIE3

@misc{pith2026250713653,
  author       = {Pith},
  title        = {Pith review of: Coupled Modeling of External Pressure and Capillary Blood Flow: Nonlinear Dynamics of Vascular Elasticity and Collapse Effects},
  year         = {2026},
  howpublished = {\url{https://pith.science/paper/KNA6WIE3}},
  note         = {Machine review of arXiv:2507.13653}
}
read the original abstract

External pressure significantly influences microcirculatory capillary blood flow, yet current studies lack quantitative modeling. This work proposes a nonlinear segmented coupling model between external pressure and capillary flow, incorporating vascular elasticity and collapse effects. The pressure-flow response is divided into three phases: elastic compression under low pressure (less than 30 mmHg), elliptical collapse in the transition zone (30 to 40 mmHg), and closure-induced attenuation under high pressure (above 40 mmHg), with explicit expressions derived for each. Parameter sensitivity analysis and comparison with literature demonstrate the model's capability in capturing key determinants. The proposed framework supports dose-response assessment and individualized parameter tuning in pressure-based therapies such as tourniquets and compression garments.

Discussion (0). Continue with ORCID to comment.

Reference graph

Works this paper leans on

36 extracted references · 36 canonical work pages

  1. [1]

    International Journal of Nonlinear Analysis and Applications 13(1), 1341–1350 (2022)

    Abdullah, E.Y.: Study of pressure applied to blood vessels using a mathemati- cal model. International Journal of Nonlinear Analysis and Applications 13(1), 1341–1350 (2022)

    work page 2022

  2. [2]

    In: Seminars in Thrombosis and Hemostasis, vol

    Baskurt, O.K., Meiselman, H.J.: Blood rheology and hemodynamics. In: Seminars in Thrombosis and Hemostasis, vol. 50, pp. 902–915 (2024). Thieme Medical

    work page 2024

  3. [3]

    Journal of Investigative Dermatol- ogy Symposium Proceedings 5(1), 3–9 (2000)

    Braverman, I.M.: The cutaneous microcirculation. Journal of Investigative Dermatol- ogy Symposium Proceedings 5(1), 3–9 (2000)

    work page 2000

  4. [4]

    Plastic and Reconstructive Surgery 143(2), 310–321 (2019)

    Bailey, J.K., Powell, H.M.: Role of early application of pressure garments following burn injury and autografting. Plastic and Reconstructive Surgery 143(2), 310–321 (2019)

    work page 2019

  5. [5]

    Archives of Hand and Microsurgery 26(4), 285–292 (2021) Dharmangadan Sree, V.: Multiscale and multiphysics modeling of pressure driven ischemia and ulcer formation in the skin

    Doh, G., Kim, B., Lee, D., Yoon, J., Lim, S., Han, Y.S., Eo, S.: Hemodynamic prin- ciples in free tissue transfer: Vascular changes at the anastomosis site. Archives of Hand and Microsurgery 26(4), 285–292 (2021) Dharmangadan Sree, V.: Multiscale and multiphysics modeling of pressure driven ischemia and ulcer formation in the skin. PhD thesis, Purdue Univ...

    work page 2021

  6. [6]

    Symmetry 13(6), 1020 (2021)

    Farina, A., Fasano, A., Rosso, F.: Mathematical models for some aspects of blood microcirculation. Symmetry 13(6), 1020 (2021)

    work page 2021

  7. [7]

    Journal of Non-Newtonian Fluid Mechanics 287, 104464 (2021)

    Fusi, L., Farina, A., Saccomandi, G.: Linear stability analysis of the poiseuille flow of a stratified non-newtonian suspension: Application to microcirculation. Journal of Non-Newtonian Fluid Mechanics 287, 104464 (2021)

    work page 2021

  8. [8]

    Springer, New York (2013)

    Fung, Y.-c.: Biomechanics: Mechanical Properties of Living Tissues. Springer, New York (2013)

    work page 2013

Show all 36 references
  1. [9]

    Blood Purification 49(1-2), 143–150 (2020)

    Guven, G., Hilty, M.P., Ince, C.: Microcirculation: physiology, pathophysiology, and clinical application. Blood Purification 49(1-2), 143–150 (2020)

    2020

  2. [10]

    Garg, A., Mishra, H., Pattanayek, S.K.: Optimal flow and scaling laws for power-law 15 fluids in elliptical cross-section self-similar tree-like networks (2024)

    2024

  3. [11]

    Composites Part B: Engineering 35(6-8), 591–598 (2004)

    Han, J.H., Kardomateas, G.A., Simitses, G.J.: Elasticity, shell theory and finite ele- ment results for the buckling of long sandwich cylindrical shells under external pressure. Composites Part B: Engineering 35(6-8), 591–598 (2004)

    2004

  4. [12]

    Journal of the Mechanics and Physics of Solids 186, 105605 (2024)

    Huang, W.Z., Li, B., Feng, X.Q.: Mechanobiological tortuosity of blood vessels with stress-modulated growth and remodeling. Journal of the Mechanics and Physics of Solids 186, 105605 (2024)

    2024

  5. [13]

    Journal of Biomedical Optics24(8), 080901 (2019)

    Heeman, W., Steenbergen, W., Dam, G.M., Boerma, E.C.: Clinical applications of laser speckle contrast imaging: a review. Journal of Biomedical Optics24(8), 080901 (2019)

    2019

  6. [14]

    In: Coro- nary Circulation: Anatomy, Mechanical Properties, and Biomechanics, pp

    Kassab, G.S., Kassab, G.S.: Constitutive models of coronary vasculature. In: Coro- nary Circulation: Anatomy, Mechanical Properties, and Biomechanics, pp. 173–308 (2019)

    2019

  7. [15]

    Annals of Biomedical Engineering 35, 2095–2107 (2007)

    Linder-Ganz, E., Gefen, A.: The effects of pressure and shear on capillary closure in the microstructure of skeletal muscles. Annals of Biomedical Engineering 35, 2095–2107 (2007)

    2007

  8. [16]

    Advances in Skin & Wound Care 21(6), 282–292 (2008)

    Langemo, D., Thompson, P., Hunter, S., Hanson, D., Anderson, J.: Heel pressure ulcers: stand guard. Advances in Skin & Wound Care 21(6), 282–292 (2008)

    2008

  9. [17]

    basic concepts

    Loiseau, E., Viallat, A., Abkarian, M.: Blood in flow. basic concepts. In: Dynamics of Blood Cell Suspensions in Microflows, pp. 1–39. CRC Press, Boca Raton, FL (2019)

    2019

  10. [18]

    American Journal of Physiology-Heart and Circulatory Physiology 323(5), 1019–1036 (2022)

    Murrant, C.L., Fletcher, N.M.: Capillary communication: the role of capillaries in sens- ing the tissue environment, coordinating the microvascular, and controlling blood flow. American Journal of Physiology-Heart and Circulatory Physiology 323(5), 1019–1036 (2022)

    2022

  11. [19]

    World 1(3), 13–23 (2012)

    Negosanti, L., Pinto, V., Sgarzani, R., Negosanti, F., Zannetti, G., Cipriani, R.: World journal of. World 1(3), 13–23 (2012)

    2012

  12. [20]

    Archives of Pharmacy Practice 14(2-2023), 70–74 (2023)

    Orusbiev, A.R., Alunkacheva, T.G., Charandaeva, M.S., Kireeva, B.S., Gadzhiev, M.F., Zelenetckii, V.G.: Study of the structural and mechanical properties of ery- throcyte membranes using atomic force microscopy. Archives of Pharmacy Practice 14(2-2023), 70–74 (2023)

    2023

  13. [21]

    Master’s thesis, Aalto University (2022)

    Panula, T.: Blood pressure and hemodynamic monitoring from the fingertip. Master’s thesis, Aalto University (2022)

    2022

  14. [22]

    Arteriosclerosis, Thrombosis, and Vascular Biology 39(11), 233–243 (2019)

    Peng, Z., Shu, B., Zhang, Y., Wang, M.: Endothelial response to pathophysiological stress. Arteriosclerosis, Thrombosis, and Vascular Biology 39(11), 233–243 (2019)

    2019

  15. [23]

    European Journal of Vascular and Endovascular Surgery 57(2), 276–282 (2019)

    Rastel, D., Lun, B.: Lower limb deep vein diameters beneath medical compression 16 stockings in the standing position. European Journal of Vascular and Endovascular Surgery 57(2), 276–282 (2019)

    2019

  16. [24]

    Physiological Reports 10(10), 15303 (2022)

    Roy, T.K., Secomb, T.W.: Functional implications of microvascular heterogeneity for oxygen uptake and utilization. Physiological Reports 10(10), 15303 (2022)

    2022

  17. [25]

    Cureus 12(2) (2020)

    Sloop, G.D., De Mast, Q., Pop, G., Weidman, J.J., Cyr, J.A.S.: The role of blood viscosity in infectious diseases. Cureus 12(2) (2020)

    2020

  18. [26]

    International Journal for Numerical Methods in Biomedical Engineering 35(12), 3277 (2019)

    Sharzehee, M., Fatemifar, F., Han, H.C.: Computational simulations of the helical buckling behavior of blood vessels. International Journal for Numerical Methods in Biomedical Engineering 35(12), 3277 (2019)

    2019

  19. [27]

    Frontiers in Physiology 12, 712636 (2021)

    Seddighi, Y., Han, H.C.: Buckling of arteries with noncircular cross sections: theory and finite element simulations. Frontiers in Physiology 12, 712636 (2021)

    2021

  20. [28]

    Polish Archives of Internal Medicine 130(2), 130–139 (2020)

    Stompor, T., Perkowska-Ptasi´ nska, A.: Hypertensive kidney disease: a true epidemic or rare disease. Polish Archives of Internal Medicine 130(2), 130–139 (2020)

    2020

  21. [29]

    Biomechanics and Modeling in Mechanobiology 18, 1947–1964 (2019)

    Sree, V.D., Rausch, M.K., Tepole, A.B.: Linking microvascular collapse to tissue hypoxia in a multiscale model of pressure ulcer initiation. Biomechanics and Modeling in Mechanobiology 18, 1947–1964 (2019)

    2019

  22. [30]

    Advanced Functional Materials 34(1), 2305245 (2024)

    Song, B., Wang, C., Fan, S., Zhang, L., Zhang, C., Xiong, W., Li, J.: Rapid construc- tion of 3d biomimetic capillary networks with complex morphology using dynamic holographic processing. Advanced Functional Materials 34(1), 2305245 (2024)

    2024

  23. [31]

    Journal of the Mechanics and Physics of Solids 174, 105274 (2023)

    Sun, W.K., Yin, B.B., Zhang, L.W., Liew, K.M.: Blood pressure-driven rupture of blood vessels. Journal of the Mechanics and Physics of Solids 174, 105274 (2023)

    2023

  24. [32]

    Metabolism 43(1S), 84–197 (2023)

    Tagliabue, S.e.a.: Microvascular cerebral blood flow dynamics for intracranial pressure estimates: transcranial diffuse correlation spectroscopy. Metabolism 43(1S), 84–197 (2023)

    2023

  25. [33]

    Digital Medicine 5(4), 141–153 (2019)

    Thiriet, M.: Input data for computational models of blood flows. Digital Medicine 5(4), 141–153 (2019)

    2019

  26. [34]

    In: Clinically Applied Microcirculation Research, pp

    Tooke, J.E., Smaje, L.H.: The microcirculation and clinical disease. In: Clinically Applied Microcirculation Research, pp. 3–16. Routledge, London (2019)

    2019

  27. [35]

    In: Cerebral Venous System in Acute and Chronic Brain Injuries, pp

    Tong, L.S., Yu, Y.N., Tang, J., Lou, M., Zhang, J.H.: Involvement of cerebral venous system in ischemic stroke. In: Cerebral Venous System in Acute and Chronic Brain Injuries, pp. 195–205 (2019)

    2019

  28. [36]

    Current Hepatology Reports 19, 40–53 (2020) 17

    Wanless, I.R.: The role of vascular injury and congestion in the pathogenesis of cir- rhosis: the congestive escalator and the parenchymal extinction sequence. Current Hepatology Reports 19, 40–53 (2020) 17

    2020

Pith tools

Reviewed August 6, 2026 · model on record in the stance chip above.