Post-ischemic Reperfusion
Post-ischemic Reperfusion - Related Videos
09:09
Ischemia-reperfusion Model of Acute Kidney Injury and Post Injury Fibrosis in Mice
0 Views •
Cited by 141 •
2013
We describe models of moderate and severe ischemia-reperfusion-induced kidney injury in which the mice undergo unilateral renal pedicle clamping followed by simultaneous or delayed contralateral nephrectomy, respectively. These models consistently give rise to renal dysfunction and post-injury fibrosis, but injury severity and survival are dependent on mouse background, age and surgical equipment.
07:07
Murine Model of Intestinal Ischemia-reperfusion Injury
0 Views •
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
0 Views •
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.
06:29
Inducing Ischemia-reperfusion Injury in the Mouse Ear Skin for Intravital Multiphoton Imaging of Immune Responses
0 Views •
Cited by 15 •
2016
This protocol describes the induction of an ischemia-reperfusion (IR) model on mouse ear skin using magnet clamping. Using a custom-built intravital imaging model, we study in vivo inflammatory responses post-reperfusion. The rationale behind the development of this technique is to extend the understanding of how leukocytes respond to skin IR injury.
09:15
Stem Cell Transplantation in an in vitro Simulated Ischemia/Reperfusion Model
0 Views •
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.
FAQs
Reoxygenation can produce a rapid increase in reactive oxygen species, chemically reactive molecules that promote oxidative stress. At the same time, cells may lose calcium control, mitochondria may function poorly, and inflammatory pathways may become active. These responses can damage cellular structures and the endothelium, the vessel lining, so restored circulation does not always produce immediate tissue recovery.
Reperfusion disrupts calcium balance while impairing mitochondrial function, creating two linked sources of cellular stress. Mitochondrial impairment limits normal energy-related activity and can accompany the oxidative stress that follows renewed oxygen delivery. Together, these disturbances help explain why reoxygenation may amplify injury in cells that were already stressed by ischemia.
Endothelial injury adds vascular damage to the original cellular effects of ischemia. Because the endothelium forms the inner lining of blood vessels, its impairment represents a separate consequence of oxidative stress and inflammation during reperfusion. This makes vascular injury an important part of understanding why restored circulation can produce both tissue rescue and additional harm.
Treatment research must address a therapeutic balance: restoring oxygen delivery can rescue injured cells, yet the same transition can initiate oxidative, mitochondrial, calcium-related, inflammatory, and endothelial damage. Studies therefore aim to limit reperfusion injury without preventing tissue recovery. This balance shapes efforts to improve strategies and outcomes after interrupted circulation.
The response is relevant whenever circulation has been interrupted and then restored, including stroke, myocardial infarction, organ transplantation, and shock. These settings differ clinically, but each makes the consequences of renewed blood flow important to medical care. Understanding the shared injury mechanisms provides context for evaluating approaches intended to preserve recovery while reducing additional tissue damage.
Researchers seek strategies that preserve the beneficial recovery associated with renewed blood flow while reducing oxidative stress, calcium disruption, mitochondrial impairment, inflammation, and endothelial injury. The desired outcome is not simply restored circulation, but better tissue recovery after ischemia. This research context connects cellular mechanisms with improved therapeutic strategies for conditions involving interrupted circulation.