Ischemia-reperfusion Model
Ischemia-reperfusion Model - Related Videos
07:07
Murine Model of Intestinal Ischemia-reperfusion Injury
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Cited by 52 •
2016
Here we describe the detailed procedure of intestinal ischemia-reperfusion in mice which results in reproducible injury without mortality to encourage the standardization of this technique across the field. This model of intestinal ischemia-reperfusion injury can be utilized to study the cellular and molecular mechanisms of injury and regeneration.
13:42
A Murine Closed-chest Model of Myocardial Ischemia and Reperfusion
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Cited by 19 •
2012
Surgical trauma induces an inflammatory response. Cytokines and endogenous ligands are known to modulate myocardial infarct size following ischemia and reperfusion. We present a modified closed-chest model of murine ischemia and reperfusion using hanging weights to minimize effects of thoracotomy.
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.
09:15
Stem Cell Transplantation in an in vitro Simulated Ischemia/Reperfusion Model
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Cited by 3 •
2011
We demonstrate how to set up an in vitro ischemia/reperfusion model and how to evaluate the effect of stem cell therapy on postischemic cardiac cells.
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.
FAQs
Restoring blood flow can intensify injury through several connected processes rather than simply reversing ischemic damage. Reactive oxygen species increase oxidative stress, while mitochondrial dysfunction further impairs cellular energy handling. In parallel, inflammatory responses and endothelial injury can worsen tissue disruption. Studying these interacting mechanisms helps researchers identify which events might be targeted to preserve tissue after blood flow returns.
Mitochondrial dysfunction links oxygen deprivation with the tissue damage observed after flow is restored. Ischemia disrupts cellular energy production, and reperfusion may amplify this disturbance through reactive oxygen species. Examining mitochondrial effects therefore helps distinguish metabolic injury from the broader inflammatory and endothelial responses, providing a mechanistic basis for evaluating treatments intended to limit cellular damage.
The model separates the period of interrupted blood supply from the subsequent restoration phase, allowing investigators to examine their different contributions to tissue injury. Ischemia emphasizes oxygen and nutrient deprivation, whereas reperfusion highlights reactive oxygen species, mitochondrial dysfunction, inflammation, and endothelial injury. This distinction supports more precise analysis of when protective interventions may be most effective.
A typical study establishes a temporary interruption of blood supply, restores flow, and then evaluates the resulting tissue response. Investigators can assess tissue damage alongside functional recovery and inflammatory responses, rather than relying on a single endpoint. This workflow connects the timing of ischemia and reperfusion with measurable biological outcomes and supports comparison of protective strategies.
The model is applied to the heart, brain, kidney, and liver, where temporary loss and restoration of blood supply can produce clinically important injury. Organ-specific studies examine how tissue damage, functional recovery, and inflammatory responses develop in each setting. These applications provide experimental context for conditions including myocardial infarction, stroke, transplantation, and trauma.
Researchers can determine whether an intervention reduces tissue damage, improves functional recovery, or limits inflammatory responses after blood flow is restored. The same experimental framework also supports evaluation of surgical strategies and therapies designed to reduce reperfusion injury. Results are especially relevant when developing approaches for stroke, myocardial infarction, transplantation, or trauma-related tissue damage.