Related Experiment Video

Updated: Feb 13, 2026

Focal Cerebral Ischemia Model by Endovascular Suture Occlusion of the Middle Cerebral Artery in the Rat
13:50

Focal Cerebral Ischemia Model by Endovascular Suture Occlusion of the Middle Cerebral Artery in the Rat

Published on: February 5, 2011

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Downstream Microvascular Thrombosis in Cortical Venules Is an Early Response to Proximal Cerebral Arterial Occlusion

Jean-Philippe Desilles1,2, Varouna Syvannarath1, Lucas Di Meglio1

  • 1Laboratory for Vascular Translational Science, Inserm Unit 1148, Sorbonne Paris Cite University Paris Diderot, Paris, France.

Journal of the American Heart Association
|March 3, 2018
PubMed
Abstract

Insights

Downstream microvascular thromboinflammation, involving leukocytes and fibrinogen, initiates rapidly after acute ischemic stroke and contributes to incomplete reperfusion and delayed brain bleeding. This process is critical in stroke pathophysiology.

Area of Science:

  • Neuroscience
  • Vascular Biology
  • Pathophysiology

Background:

  • Acute ischemic stroke involves downstream microvascular thromboinflammation contributing to brain damage.
  • Understanding the precise sequence of these events is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate and characterize the temporal sequence of downstream microvascular thromboinflammation in an acute ischemic stroke model.
  • To elucidate the role of leukocytes, platelets, and fibrinogen in this process.

Main Methods:

  • Rats underwent transient middle cerebral artery (MCA) occlusion to model ischemic stroke.
  • Real-time intravital imaging and laser Doppler interferometry were used to analyze cerebral microcirculation.
  • Fluorescent markers tracked leukocytes, platelets, fibrinogen, and blood-brain barrier permeability.

Main Results:

  • MCA occlusion caused immediate drops in microvascular blood flow and leukocyte margination in venules.
  • Leukocyte margination promoted fibrinogen deposition and thrombosis, impairing blood flow restoration.
  • Blood-brain barrier disruption and leukocyte extravasation persisted, leading to delayed microhemorrhages.

Conclusions:

  • Microvascular thrombosis and blood-brain barrier disruption begin immediately after MCA occlusion and propagate via the venous system.
  • Leukocyte margination is central to initiating and propagating thromboinflammation.
  • This thromboinflammatory cascade underlies incomplete reperfusion and delayed microhemorrhages post-stroke.
Keywords:
blood–brain barrierleukocytemiddle cerebral artery occlusionno‐reflowvenous thrombosis

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