Transient Cca Occlusion
Transient Cca Occlusion - Related Videos
03:44
Filament Insertion-based Transient Stroke Model: A Surgical Procedure to Perform Middle Cerebral Artery Occlusion in Murine Brain
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2025
This video describes the procedure to develop transient stroke in a murine model using silicon-coated filament-based occlusion of the middle cerebral artery. The developed model mimics human stroke, thus helping to investigate novel therapeutic strategies for treating stroke.
05:32
Transient Middle Cerebral Artery Occlusion Model of Stroke
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Cited by 9 •
2023
This protocol describes the model of transient focal cerebral ischemia in mice through intraluminal occlusion of the middle cerebral artery. Additionally, examples of outcome assessment are shown using magnetic resonance imaging and behavioral tests.
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.
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.
09:48
Quantification of Neurovascular Protection Following Repetitive Hypoxic Preconditioning and Transient Middle Cerebral Artery Occlusion in Mice
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Cited by 14 •
2015
This protocol describes repetitive hypoxic preconditioning, or brief exposures to systemic hypoxia that reduce infarct volumes and blood-brain barrier disruption following transient middle cerebral artery occlusion in mice. It also details dual quantification of infarct volume and blood-brain barrier disruption after stroke to assess the efficacy of neurovascular protection.
FAQs
The central mechanism is a controlled reduction in cerebral perfusion. Interrupting common carotid artery flow limits blood supply to the brain, allowing investigators to examine cerebrovascular responses and changes associated with temporary ischemia. Because circulation is subsequently restored, the same model also exposes recovery-related processes rather than only the effects of sustained vascular obstruction.
Reperfusion provides a defined period in which circulation returns after the occlusion is released. This makes it possible to study how the brain responds not only during reduced blood supply but also during recovery. Researchers can therefore investigate processes associated with ischemia-reperfusion, including recovery patterns, neuronal injury, inflammation, and other physiological changes.
This approach supports examination of several responses to temporary cerebral hypoperfusion. These include cerebrovascular reactions, neuronal injury, inflammatory changes, and recovery after blood flow is restored. Considering these outcomes together helps researchers relate altered circulation to both immediate brain effects and subsequent biological responses within a controlled ischemia-reperfusion setting.
The procedure follows a defined sequence: an occlusive method, typically a vascular clamp or another suitable approach, interrupts common carotid artery flow for a specified interval. The occlusion is then released, restoring circulation. This sequence establishes the temporary ischemic phase and the subsequent reperfusion phase needed for structured physiological and neurological investigation.
Researchers can use the model to examine whether a treatment changes outcomes associated with temporary ischemia and subsequent reperfusion. Comparisons may focus on neuronal injury, inflammatory responses, cerebrovascular behavior, or recovery-related changes. In this way, the procedure provides a controlled context for assessing protective mechanisms and potential therapeutic effects in biomedical research.
A defined interval makes the reduction in arterial flow a controlled experimental condition rather than an uncontrolled event. Investigators can relate observed cerebrovascular, neuronal, inflammatory, or recovery-related changes to a specified period of ischemia before circulation is restored. This structure helps organize measurements across the ischemic and reperfusion phases of the study.