Mouse Ischemia Model
Mouse Ischemia Model - Related Videos
07:37
A Mouse Model of Retinal Ischemia-Reperfusion Injury Through Elevation of Intraocular Pressure
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Cited by 102 •
2016
This article describes a procedure for inducing retinal ischemia-reperfusion injury by elevated intraocular pressure in mice. Retinal ischemia-reperfusion injury by elevated intraocular pressure serves to model human pathologies characterized by compromised oxygen and nutrient delivery in the retina, enabling researchers to examine potential cellular mechanisms and treatments for human diseases of the retinal neurovascular unit.
02:42
Inducing Thrombotic Stroke Through Hypoxia and Ischemia in a Mouse Model
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2025
This video demonstrates the procedure of replicating a thrombotic stroke in a mouse model by blocking the right common carotid artery and exposing the mouse to a low-oxygen environment. This process reduces blood and oxygen flow to the brain, causing blood clot formation and brain damage.
12:51
Murine Model of Hindlimb Ischemia
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Cited by 201 •
2009
The surgical procedure for induction of unilateral hindlimb ischemia is demonstrated, with confirmation of ischemia by laser Doppler perfusion imaging.
02:29
Assessing the Neuroprotective Effects of Acidic Postconditioning in a Mouse Model of Cerebral Ischemia
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2025
Source: Zheng, Y., et al. Experimental Models to Study the Neuroprotection of Acidic Postconditioning Against Cerebral Ischemia. J. Vis. Exp. (2017)This video demonstrates the application of acidic postconditioning (APC) to evaluate its neuroprotective effects against ischemic injury in a mouse model of middle cerebral artery occlusion (MCAO). It outlines the steps involved in reperfusion in the MCAO model and the application of APC during reperfusion to mitigate excitotoxicity, oxidative...
10:25
Normothermic Cardiac Arrest and Cardiopulmonary Resuscitation: A Mouse Model of Ischemia-Reperfusion Injury
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Cited by 20 •
2011
A powerful model for perioperative and critical care related acute kidney injury is presented. Using whole body hypoperfusion induced by cardiac arrest it is possible to nearly replicate the histologic and functional changes of clinical AKI.
FAQs
Occlusion duration and reperfusion are major determinants of injury severity. A longer blockage can produce a more severe ischemic insult, while restoring flow after temporary occlusion creates a different experimental condition from maintaining a permanent blockage. Controlling these variables helps researchers generate defined injury patterns and compare how blood-flow interruption affects infarct development, neuronal injury, inflammation, and recovery.
Temporary occlusion blocks the middle cerebral artery for a defined period before blood flow is restored, whereas permanent occlusion maintains the blockage. These approaches model different vascular conditions and can produce different injury profiles. Selecting one or the other allows investigators to examine responses to persistent ischemia or to the combination of reduced flow followed by reperfusion within the same experimental framework.
The model links an initial vascular event with consequences at several biological levels. Reduced arterial flow produces an ischemic region, followed by measurable neuronal injury and inflammation. Researchers can then relate these tissue responses to behavioral deficits and later brain recovery. This progression makes the system useful for studying how vascular disruption becomes cellular damage and functional impairment.
Evaluation can combine structural, cellular, inflammatory, and functional outcomes. Researchers may assess infarct development to estimate the affected tissue, neuronal injury to examine cellular damage, inflammation to characterize the tissue response, and behavioral deficits to determine functional impact. Considering several readouts together provides a broader view of injury severity and helps identify whether an intervention supports neuroprotection or recovery.
A typical workflow uses a filament to block the middle cerebral artery in a mouse, with the blockage maintained temporarily or permanently according to the study design. In temporary experiments, blood flow is subsequently restored. Investigators then examine outcomes such as infarct development, neuronal injury, inflammation, behavioral deficits, and brain recovery to characterize the resulting ischemic injury.
Researchers use the model when they need to test how a candidate therapy affects stroke-related injury or recovery in vivo. Treatment effects can be examined through infarct development, neuronal injury, inflammation, and behavioral deficits. The same framework also supports evaluation of neuroprotective strategies that limit damage and restorative strategies intended to improve outcomes during brain recovery.
Mice allow investigators to study cerebral ischemia under controlled genetic and physiological conditions. This control helps researchers connect differences in biological background or physiological state with vascular injury, cellular responses, and functional outcomes. In neuroscience, that capability supports experiments linking blood-flow disruption to mechanisms of brain damage and recovery while also providing a controlled setting for testing therapeutic strategies.