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Related Concept Videos

Vascular Spasm01:16

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The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last...
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Stretch in Brain Microvascular Endothelial Cells cEND as an In Vitro Traumatic Brain Injury Model of the Blood Brain Barrier
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Cerebrovascular dysfunction following subfailure axial stretch.

E David Bell1, Anthony J Donato2, Kenneth L Monson1

  • 1Department 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.

Journal of the Mechanical Behavior of Biomedical Materials
|October 14, 2016
PubMed
Summary
This summary is machine-generated.

Traumatic brain injury can damage cerebral blood vessels through mechanical stretch, altering vascular smooth muscle cell function. Rapid, high-level overstretch significantly impairs vessel contraction and response to stimuli, persisting for an hour post-injury.

Keywords:
Autoregulatory dysfunctionDamageRat cerebral blood vesselsTraumatic brain injury

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Area of Science:

  • Biomedical Engineering
  • Neuroscience
  • Vascular Physiology

Background:

  • Cerebral blood vessels are crucial for brain health, but traumatic brain injury (TBI) often causes autoregulatory dysfunction.
  • While biochemical changes post-TBI are known, direct effects of tissue deformation on vascular smooth muscle cells (SMCs) remain less understood.
  • Understanding mechanical stress on cerebral vessels is vital for TBI research.

Purpose of the Study:

  • To investigate the impact of axial overstretch on the contractile behavior of SMCs in rat middle cerebral arteries (MCAs).
  • To determine if stretch and strain rate thresholds exist for altering SMC function.
  • To differentiate mechanical effects from biochemical factors in TBI-related vascular dysfunction.

Main Methods:

  • Isolated rat MCAs were subjected to varying levels of axial overstretch (1.2*λIV or 1.3*λIV) at different strain rates (0.2 or 20s⁻¹).
  • Vascular smooth muscle cell contractile responses to potassium (K+) were measured before and after overstretch.
  • Key metrics included percent contraction (%C) and the K+ dose for half-maximal response (EC50), analyzed relative to controls.

Main Results:

  • Axial overstretch significantly altered SMC contractile behavior, specifically a decrease in %C and an increase in EC50.
  • These functional changes were observed only in vessels subjected to rapid (20s⁻¹) overstretch to 1.3*λIV.
  • The reduction in %C was immediate, while the increase in EC50 persisted for 60 minutes post-overstretch.

Conclusions:

  • Mechanical deformation, particularly rapid and high-level axial overstretch, directly impairs SMC contractile function in MCAs.
  • This suggests that tissue deformation plays a significant role in cerebrovascular autoregulatory dysfunction following TBI.
  • These findings highlight a mechanical mechanism contributing to TBI-induced vascular issues, independent of biochemical changes.