Permanent Focal Ischemia
Permanent Focal Ischemia - Related Videos
09:59
A Magnetic Resonance Imaging Protocol for Stroke Onset Time Estimation in Permanent Cerebral Ischemia
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Cited by 17 •
2017
A protocol for stroke onset time estimation in a rat model of stroke exploiting quantitative magnetic resonance imaging (qMRI) parameters is described. The procedure exploits diffusion MRI for delineation of the acute stroke lesion and quantitative T1 and T2 (qT1 and qT2) relaxation times for timing of stroke.
07:46
Bilateral Common Carotid Artery Occlusion as an Adequate Preconditioning Stimulus to Induce Early Ischemic Tolerance to Focal Cerebral Ischemia
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Cited by 30 •
2013
There is accumulating evidence, that ischemic preconditioning (PC) – a non-damaging ischemic challenge to the brain - confers a transient protection to a subsequent damaging ischemic insult. We established bilateral common carotid artery occlusion (BCCAO) as a preconditioning stimulus to induce early ischemic tolerance (IT) to transient focal cerebral ischemia (induced by middle cerebral artery occlusion, MCAO) in C57Bl6/J mice.
08:27
Photothrombosis-induced Focal Ischemia as a Model of Spinal Cord Injury in Mice
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Cited by 3 •
2015
Photothrombosis is a minimally invasive and highly reproducible procedure to induce focal ischemia in the spinal cord and serves as a model of spinal cord injury in mice.
13:50
Focal Cerebral Ischemia Model by Endovascular Suture Occlusion of the Middle Cerebral Artery in the Rat
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Cited by 107 •
2011
Surgical induction of ischemic brain damage in the rat is a widely used model for stroke research. Here we demonstrate the induction of focal cerebral ischemia by occlusion of the middle cerebral artery. Visualization of the resulting infarct by histological staining and magnetic resonance imaging is also shown.
08:27
The Application Of Permanent Middle Cerebral Artery Ligation in the Mouse
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Cited by 29 •
2011
Middle cerebral artery (MCA) ligation is a technique to study focal cerebral ischemia in animal models. In this method, the middle cerebral artery is exposed by craniotomy and ligated by cauterization. This method gives highly reproducible infarct volumes and increased post-operative survival rates compared to other methods available.
FAQs
The central injury sequence begins when oxygen and glucose deprivation limits ATP production. ATP depletion disrupts membrane energy balance and causes depolarization, while glutamate-driven excitotoxicity further stresses neurons. These linked events promote cellular injury and help explain why the model is valuable for examining mechanisms that make ischemic damage progressively difficult to reverse.
The ischemic core represents tissue experiencing the most severe injury, while the surrounding penumbra marks tissue affected by the evolving ischemic process. Studying both regions allows researchers to track how damage develops beyond the initial site of greatest injury. This distinction supports analysis of infarct progression and regional differences in neuronal and vascular responses.
Because blood flow is not restored, Permanent Focal Ischemia emphasizes the mechanisms of sustained and irreversible injury rather than the effects of reperfusion. This condition helps researchers examine how injury continues over time, including progression from the ischemic core into penumbral tissue and the biological processes associated with lasting neurological damage.
The experimental model begins with arterial occlusion that produces a localized, sustained reduction in blood flow. Researchers then assess the resulting tissue injury and biological responses, including infarct development, neurovascular changes, and inflammation. Depending on the study design, these observations can be related to later functional outcomes or responses to a potential neuroprotective treatment.
Researchers can evaluate infarct development, which reflects the extent and progression of injured brain tissue. They can also analyze neurovascular responses, inflammatory activity, and longer-term functional outcomes. Together, these measurements connect tissue-level damage with changes in the surrounding biological environment and help determine whether an intervention alters the course or consequences of ischemic injury.
This model is particularly useful for studying ischemic stroke, irreversible brain injury, and the progression of damage over time. It also supports evaluation of potential neuroprotective treatments by providing measurable outcomes such as infarct development and functional consequences. Its sustained occlusion makes it relevant when researchers want to focus on injury mechanisms without blood-flow restoration.