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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...

Ischemic Stroke l: Introduction

Ischemic Stroke l: Introduction

Ischemic stroke is an acute cerebrovascular condition in which blood flow to a brain region is suddenly interrupted, leading to tissue infarction. Neurons depend on continuous oxygen and glucose supply, so even brief reductions in perfusion cause energy failure, ionic imbalance, and irreversible injury. Ischemic strokes are classified into thrombotic and embolic types based on their underlying mechanisms.Thrombotic MechanismsThrombotic stroke develops when a clot forms within a cerebral artery.

Hemorrhagic Stroke ll: Pathophysiology

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...

Hemorrhagic Stroke l: Introduction

Hemorrhagic Stroke l: Introduction

A hemorrhagic stroke is an acute neurological event that occurs when a weakened cerebral blood vessel ruptures, allowing blood to accumulate within or around the brain. The sudden release of blood forms a focal hematoma that increases intracranial pressure, displaces neural tissue, and can obstruct cerebrospinal fluid pathways. These effects may be compounded by intraventricular extension of the hemorrhage, cerebral edema, or compression of adjacent structures, all of which contribute to...

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Related Experiment Video

Updated: May 26, 2026

Non-invasive Imaging and Analysis of Cerebral Ischemia in Living Rats Using Positron Emission Tomography with 18F-FDG

Non-invasive Imaging and Analysis of Cerebral Ischemia in Living Rats Using Positron Emission Tomography with ¹⁸F-FDG

Published on: December 28, 2014

VEGF expression in human brain tissue after acute ischemic stroke.

Otilia Mărgăritescu¹, D Pirici, Cl Mărgăritescu

¹Department of Pathology, Faculty of Dentistry, University of Medicine and Pharmacy of Craiova, Romania. c_margaritescu2000@yahoo.com

Romanian Journal of Morphology and Embryology = Revue Roumaine De Morphologie Et Embryologie

|December 29, 2011

Summary

Vascular Endothelial Growth Factor (VEGF) shows significant reactivity in brain cells following ischemic stroke. This suggests potential neuroprotective and angiogenic effects, offering therapeutic possibilities for stroke patients.

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Last Updated: May 26, 2026

Non-invasive Imaging and Analysis of Cerebral Ischemia in Living Rats Using Positron Emission Tomography with 18F-FDG

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Area of Science:

Neuroscience
Pathophysiology
Biomedical Research

Background:

Ischemic stroke is a leading cause of death, necessitating research into its underlying mechanisms.
Angiogenesis, the formation of new blood vessels, is a potential strategy to enhance oxygen delivery to ischemic brain tissue.
Vascular Endothelial Growth Factor (VEGF) is a key regulator of angiogenesis.

Purpose of the Study:

To investigate the immunohistochemical expression of VEGF in various brain cellular compartments of ischemic stroke patients.
To analyze the cellular topography and intensity of VEGF immunoreactivity in relation to lesion age and type.

Main Methods:

Enzymatic immunohistochemistry was used to detect VEGF expression in brain tissue samples from 15 ischemic stroke patients and 2 controls.
Integrated optical densities (IOD) were assessed to quantify VEGF signal intensity.
Double fluorescent immunohistochemistry (VEGF with NeuN, GFAP, CD68, CD105) was performed to determine cellular localization.

Main Results:

In control brains, VEGF reactivity was observed in neurons and astrocytes.
In ischemic stroke, VEGF reactivity was present in all cell types, with the highest intensity in neurons.
VEGF expression decreased with lesion age from the infarct core outwards; astrocytes and microglia also showed reactivity, with high VEGF-CD105 colocalization in surrounding microvessels.

Conclusions:

VEGF reactivity in neurons and glial cells suggests potential neuroprotective and glial-protective roles in acute ischemic stroke.
The observed neoangiogenic properties of VEGF in microvessels surrounding infarcts may have therapeutic implications.
Further research into VEGF's role could lead to novel therapeutic strategies for ischemic stroke management.