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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.
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]
Brain ischemia has been linked to a variety of diseases or abnormalities. Individuals with sickle cell anemia, compressed blood vessels, ventricular tachycardia, plaque buildup in the arteries, blood clots, extremely low blood pressure as a result of heart attack, and congenital heart defects have a higher predisposition to brain ischemia in comparison to the average population.
After declining from 2002 to 2012, stroke death rates for middle-aged adults increased 7% between 2012 and 2019, and increased an additional 12% through 2021, the CDC found.
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.
For frostbite injuries, limiting thawing and warming of tissues until warmer temperatures can be sustained may reduce reperfusion injury. Ischemic stroke is at times treated with various levels of statin therapy at hospital discharge, followed by home time, in an attempt to lower the risk of adverse events. [28] [29]