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Reperfusion injury plays a major part in the biochemistry of hypoxic brain injury in stroke. Similar failure processes are involved in brain failure following reversal of cardiac arrest; [3] control of these processes is the subject of ongoing research.
This reperfusion results in inflammatory injury through three overlapping mechanisms. Some complimentary combination of, first, mitochondrial damage and, second, endothelial activation , causes a release of reactive oxygen species (ROS), which initiates and/or exacerbates a pathophysiological inflammatory response.
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 ...
The signs and symptoms of ischemia vary, as they can occur anywhere in the body and depend on the degree to which blood flow is interrupted. [4] For example, clinical manifestations of acute limb ischemia (which can be summarized as the "six P's") include pain, pallor, pulseless, paresthesia, paralysis, and poikilothermia.
Other symptoms may include shortness of breath, nausea, feeling faint, a cold sweat, feeling tired, and decreased level of consciousness. [1] About 30% of people have atypical symptoms. [8] Women more often present without chest pain and instead have neck pain, arm pain or feel tired. [11]
Cerebral hyperperfusion syndrome, also known as reperfusion syndrome, is a dysregulated state of cerebral blood flow following the restoration of arterial blood flow to the brain, usually following treatment of carotid artery stenosis. [1]
reperfusion [7] of previously ischemic tissue that is associated with reperfusion-related diseases, [8] such as myocardial infarction, stroke (cerebral infarction), shock-resuscitation, replantation surgery, frostbite, burns, and organ transplantation. Micrograph of testis showing hemorrhagic infarction. H&E stain.
Functional no reflow phenomenon occurs when the microvasculature is anatomically intact, but has been temporarily compromised due to spasm, microembolization, or reperfusion injury, ultimately leading to MVO. Functional no reflow phenomenon is largely reversible due to the fact that the microvasculature is still intact.