Convective forces contribute to post‐traumatic degeneration after spinal cord injury

Abstract Spinal cord injury (SCI) initiates a complex cascade of chemical and biophysical phenomena that result in tissue swelling, progressive neural degeneration, and formation of a fluid‐filled cavity. Previous studies show fluid pressure above the spinal cord (supraspinal) is elevated for at lea...

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Main Authors: Hoi Y. Kwon, Christopher Streilein, R. Chase Cornelison
Format: Article
Language:English
Published: Wiley 2025-03-01
Series:Bioengineering & Translational Medicine
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Online Access:https://doi.org/10.1002/btm2.10739
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author Hoi Y. Kwon
Christopher Streilein
R. Chase Cornelison
author_facet Hoi Y. Kwon
Christopher Streilein
R. Chase Cornelison
author_sort Hoi Y. Kwon
collection DOAJ
description Abstract Spinal cord injury (SCI) initiates a complex cascade of chemical and biophysical phenomena that result in tissue swelling, progressive neural degeneration, and formation of a fluid‐filled cavity. Previous studies show fluid pressure above the spinal cord (supraspinal) is elevated for at least 3 days after injury and contributes to a phase of damage called secondary injury. Currently, it is unknown how fluid forces within the spinal cord itself (interstitial) are affected by SCI and if they contribute to secondary injury. We find spinal interstitial pressure increases from −3 mmHg in the naive cord to a peak of 13 mmHg at 3 days post‐injury (DPI) but relatively normalizes to 2 mmHg by 7 DPI. A computational fluid dynamics model predicts interstitial flow velocities up to 0.9 μm/s at 3 DPI, returning to near baseline by 7 DPI. By quantifying vascular leakage of Evans Blue dye after a cervical hemi‐contusion in rats, we confirm an increase in dye infiltration at 3 DPI compared to 7 DPI, suggestive of higher fluid velocities at the time of peak fluid pressure. In vivo expression of the apoptosis marker caspase‐3 is strongly correlated with regions of interstitial flow at 3 DPI, and exogenously enhancing interstitial flow exacerbates tissue damage. In vitro, we show overnight exposure of neuronal cells to low pathological shear stress (0.1 dynes/cm2) significantly reduces cell count and neurite length. Collectively, these results indicate that interstitial fluid flow and shear stress may play a detrimental role in post‐traumatic neural degeneration.
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spelling doaj-art-22f132dfcd0448fcb476d2122abd61582025-08-20T03:16:35ZengWileyBioengineering & Translational Medicine2380-67612025-03-01102n/an/a10.1002/btm2.10739Convective forces contribute to post‐traumatic degeneration after spinal cord injuryHoi Y. Kwon0Christopher Streilein1R. Chase Cornelison2Department of Chemical Engineering University of Massachusetts Amherst Amherst Massachusetts USADepartment of Biomedical Engineering University of Massachusetts Amherst Amherst Massachusetts USADepartment of Chemical Engineering University of Massachusetts Amherst Amherst Massachusetts USAAbstract Spinal cord injury (SCI) initiates a complex cascade of chemical and biophysical phenomena that result in tissue swelling, progressive neural degeneration, and formation of a fluid‐filled cavity. Previous studies show fluid pressure above the spinal cord (supraspinal) is elevated for at least 3 days after injury and contributes to a phase of damage called secondary injury. Currently, it is unknown how fluid forces within the spinal cord itself (interstitial) are affected by SCI and if they contribute to secondary injury. We find spinal interstitial pressure increases from −3 mmHg in the naive cord to a peak of 13 mmHg at 3 days post‐injury (DPI) but relatively normalizes to 2 mmHg by 7 DPI. A computational fluid dynamics model predicts interstitial flow velocities up to 0.9 μm/s at 3 DPI, returning to near baseline by 7 DPI. By quantifying vascular leakage of Evans Blue dye after a cervical hemi‐contusion in rats, we confirm an increase in dye infiltration at 3 DPI compared to 7 DPI, suggestive of higher fluid velocities at the time of peak fluid pressure. In vivo expression of the apoptosis marker caspase‐3 is strongly correlated with regions of interstitial flow at 3 DPI, and exogenously enhancing interstitial flow exacerbates tissue damage. In vitro, we show overnight exposure of neuronal cells to low pathological shear stress (0.1 dynes/cm2) significantly reduces cell count and neurite length. Collectively, these results indicate that interstitial fluid flow and shear stress may play a detrimental role in post‐traumatic neural degeneration.https://doi.org/10.1002/btm2.10739computational fluid dynamicsconvection enhanced deliveryfluid shear stressinterstitial fluid flowinterstitial pressuresecondary neural injury
spellingShingle Hoi Y. Kwon
Christopher Streilein
R. Chase Cornelison
Convective forces contribute to post‐traumatic degeneration after spinal cord injury
Bioengineering & Translational Medicine
computational fluid dynamics
convection enhanced delivery
fluid shear stress
interstitial fluid flow
interstitial pressure
secondary neural injury
title Convective forces contribute to post‐traumatic degeneration after spinal cord injury
title_full Convective forces contribute to post‐traumatic degeneration after spinal cord injury
title_fullStr Convective forces contribute to post‐traumatic degeneration after spinal cord injury
title_full_unstemmed Convective forces contribute to post‐traumatic degeneration after spinal cord injury
title_short Convective forces contribute to post‐traumatic degeneration after spinal cord injury
title_sort convective forces contribute to post traumatic degeneration after spinal cord injury
topic computational fluid dynamics
convection enhanced delivery
fluid shear stress
interstitial fluid flow
interstitial pressure
secondary neural injury
url https://doi.org/10.1002/btm2.10739
work_keys_str_mv AT hoiykwon convectiveforcescontributetoposttraumaticdegenerationafterspinalcordinjury
AT christopherstreilein convectiveforcescontributetoposttraumaticdegenerationafterspinalcordinjury
AT rchasecornelison convectiveforcescontributetoposttraumaticdegenerationafterspinalcordinjury