Hypoxic Ischemia
Hypoxic Ischemia - Related Videos
08:47
The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia
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Cited by 48 •
2008
The postnatal rat model for hypoxic-ischemic brain injury is a well-established model of human neonatal hypoxic ischemic encephalopathy (HIE). In this article, we describe the model of HIE in post-natal rat pups.
08:32
Neurobehavioral Assessments in a Mouse Model of Neonatal Hypoxic-ischemic Brain Injury
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Cited by 12 •
2017
We performed unilateral carotid artery occlusion on postnatal day 7-10 CD-1 mouse pups to create a neonatal hypoxic-ischemic (HI) model and investigated the effects of HI brain injury. We studied neurobehavioral functions in these mice compared to non-operated normal mice.
09:24
An Anoxia-starvation Model for Ischemia/Reperfusion in C. elegans
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Cited by 4 •
2014
A protocol is described that uses anoxia/starvation in C. elegans to model ischemia/reperfusion. Functional outcomes include increased mortality, visible abnormalities in GFP-labeled neuronal processes, and impaired behavioral responses that require neuronal function.
02:52
Neuronal Adaptation to Repetitive Hypoxic Preconditioning in Mice
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2025
Source: Poinsatte, K., et al., Quantification of Neurovascular Protection Following Repetitive Hypoxic Preconditioning and Transient Middle Cerebral Artery Occlusion in Mice. J. Vis. Exp. (2015)This video demonstrates the method of repetitive hypoxic preconditioning (RHP) by exposing a mouse to controlled hypoxia cycles before inducing an ischemic stroke. The experiment evaluates its effects on blood-brain barrier stability, neuronal adaptation, and inflammation.
06:01
A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia
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Cited by 8 •
2015
Thromboembolic stroke models are vital tools for optimizing the recanalization therapy. Here we report a murine thrombotic stroke model based on transient cerebral hypoxic-ischemic (tHI) insult, which triggers thrombosis and infarction, and responds favorably to tissue plasminogen activator (tPA)-mediated fibrinolysis in a therapeutic window similar to those in stroke patients.
FAQs
Limited oxygen restricts mitochondrial ATP production, reducing the energy available for essential cellular work. As ATP falls, ion balance becomes disrupted, which contributes to cellular swelling and impaired tissue function. This energy failure is an early mechanistic link between inadequate oxygen delivery and the downstream cellular injury observed in hypoxic-ischemic conditions.
Energy failure promotes several interacting injury pathways rather than a single isolated effect. Excitotoxicity can intensify cellular damage, while oxidative stress injures cells through chemically reactive processes. Inflammation adds another damaging response. Together, these mechanisms can amplify the initial oxygen-deprivation injury and help determine how extensively tissue function is compromised.
Reestablishing circulation is essential for recovering oxygen delivery, but the return of blood flow can also produce reperfusion injury. This means tissue damage may continue or increase after circulation is restored, rather than ending immediately when oxygen returns. Consequently, medical strategies must consider both the period of oxygen loss and the effects of reperfusion.
The duration and intensity of oxygen deprivation influence the extent of cellular and tissue injury. More severe or prolonged disruption can produce greater disturbances in energy production, ion balance, and inflammatory responses. These differences are especially important for neurological and systemic outcomes, making the timing of injury and restoration of circulation relevant to prognosis.
Understanding its cellular mechanisms helps clinicians interpret the consequences of oxygen deprivation and evaluate likely outcomes. Diagnostic and prognostic assessment must account for the resulting energy failure, cellular stress, inflammation, and possible reperfusion injury. This framework is relevant when assessing patients with ischemic stroke, cardiac arrest, or neonatal hypoxic-ischemic encephalopathy.
The process is central to ischemic stroke, cardiac arrest, and neonatal hypoxic-ischemic encephalopathy. In each setting, insufficient oxygen delivery can threaten tissue function, while the severity and timing of injury shape neurological or systemic outcomes. Its clinical importance lies in supporting assessment and the development of approaches intended to preserve tissue during oxygen loss and reperfusion.