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Ischemic Stroke ll: Pathophysiology

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...

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Related Experiment Video

Updated: Jun 16, 2026

Induction of Acute Ischemic Stroke in Mice Using the Distal Middle Artery Occlusion Technique

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Published on: December 15, 2023

Oxygen-sensitive outcomes and gene expression in acute ischemic stroke.

Cameron Rink¹, Sashwati Roy, Mahmood Khan

¹Department of Surgery, The Ohio State University Medical Center, 473 W. 12th Avenue, Columbus, OH 43210, USA.

Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism

|February 11, 2010

Summary

Supplemental oxygen administered during acute ischemic stroke (AIS) reduced lesion volume. However, oxygen given after reperfusion worsened stroke outcomes, highlighting critical timing for therapeutic oxygen in AIS.

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Last Updated: Jun 16, 2026

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Published on: June 20, 2025

Area of Science:

Neuroscience
Biomedical Engineering
Molecular Biology

Background:

Acute ischemic stroke (AIS) involves oxygen deprivation, impacting brain tissue.
Understanding oxygen's role is crucial for developing effective stroke therapies.

Purpose of the Study:

To determine optimal therapeutic conditions for supplemental oxygen in AIS.
To identify oxygen-sensitive molecular mechanisms in stroke using transcriptome-wide screening.

Main Methods:

Rodent model of transient middle cerebral artery occlusion (MCAO).
Evaluation of normobaric (NBO) and hyperbaric oxygen (HBO) during ischemia and reperfusion.
Stroke lesion quantification via MRI, tissue oxygen measurement (EPR oxymetry), and transcriptome analysis (microarray, real-time PCR).

Main Results:

Supplemental oxygen during ischemia (iNBO, iHBO) significantly reduced stroke lesion volume compared to room air (RA).
Oxygen administration after reperfusion (rNBO, rHBO) exacerbated lesion volume.
Oxygen therapy during ischemia normalized tissue oxygen levels and identified thousands of differentially expressed genes, revealing mechanisms involving reduced leukocyte accumulation and chemokine response.

Conclusions:

The timing of supplemental oxygen administration is critical in acute ischemic stroke.
Oxygen therapy during ischemia attenuates brain damage and modulates inflammatory responses.
Findings provide insights into oxygen-dependent molecular pathways in AIS, guiding future therapeutic strategies.