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The main reason for the acute phase of ischemia-reperfusion injury is oxygen deprivation and, therefore, arrest of generation of ATP (cellular energy currency) by mitochondria oxidative phosphorylation. Tissue damage due to the general energy deficit during ischemia is followed by reperfusion (increase of oxygen level) when the injury is enhanced.
Brain injury, myocardial injury, systemic ischemia/reperfusion response: Usual onset: After resuscitation from a cardiac arrest: Duration: Weeks: Causes: Global ischemia-reperfusion injury: Risk factors: Prolonged cardiac arrest: Differential diagnosis: Systemic inflammatory response syndrome: Management: Hemodynamic stabilization and ...
Ischemia-reperfusion (IR) tissue injury is the resultant pathology from a combination of factors, including tissue hypoxia, followed by tissue damage associated with re-oxygenation. IR injury contributes to disease and mortality in a variety of pathologies, including myocardial infarction , ischemic stroke , acute kidney injury , trauma ...
Ischemia results in tissue damage in a process known as ischemic cascade. The damage is the result of the build-up of metabolic waste products, inability to maintain cell membranes , mitochondrial damage, and eventual leakage of autolyzing proteolytic enzymes into the cell and surrounding tissues.
The ischemic (ischaemic) cascade is a series of biochemical reactions that are initiated in the brain and other aerobic tissues after seconds to minutes of ischemia (inadequate blood supply). [1] This is typically secondary to stroke , injury, or cardiac arrest due to heart attack .
In surgical settings, it may be related to ischemia-reperfusion injury, where the restoration of blood flow after a period of ischemia paradoxically leads to cellular damage. In the context of severe heart attacks, the massive cell death and subsequent inflammatory response may contribute to the disruption of calcium homeostasis. [1]
It has been suggested that the three fundamental factors underlying chronic wound pathogenesis are cellular and systemic changes of aging, repeated bouts of ischemia-reperfusion injury, and bacterial colonization with resulting inflammatory host response. [22]
[52] [53] For example, in a feline model of intestinal ischemia, four hours of ischemia resulted in less injury than three hours of ischemia followed by one hour of reperfusion. [51] In ST-elevation myocardial infarction (STEMI), IRI contributes up to 50% of final infarct size despite timely primary percutaneous coronary intervention.