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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.
Cerebral ischemia/reperfusion (I/R) injury is the main pathophysiological process present in ischemic stroke. Apelin regulates many physiological functions including cardiovascular function, endocrine function, nervous system function, and feeding behavior.
Brain ischemia is insufficient blood flow to the brain, and can be acute or chronic. Acute ischemic stroke is a neurological emergency typically caused by a blood clot blocking blood flow in a vessel in the brain. [15] Chronic ischemia of the brain may result in a form of dementia called vascular dementia. [16]
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.
The caspase-dependent apoptosis cascade is initiated, causing cells to "commit suicide." If the cell dies through necrosis, it releases glutamate and toxic chemicals into the environment around it. Toxins poison nearby neurons, and glutamate can overexcite them. If and when the brain is reperfused, a number of factors lead to reperfusion injury.
Animal models of ischemic stroke are procedures inducing cerebral ischemia.The aim is the study of basic processes or potential therapeutic interventions in this disease, and the extension of the pathophysiological knowledge on and/or the improvement of medical treatment of human ischemic stroke.
Cerebral hypoxia is hypoxia specifically involving the brain. The four categories of cerebral hypoxia in order of increasing severity are: diffuse cerebral hypoxia (DCH), focal cerebral ischemia, cerebral infarction, and global cerebral ischemia. Prolonged hypoxia induces neuronal cell death via apoptosis, resulting in a hypoxic brain injury ...
Pharmacological inhibition of PFKFB3 in vitro also protects neurons from apoptosis induced by NMDAR overexcitation as well as from amyloid-ß peptide-induced neurotoxicity. When used in vivo in a mouse model of ischaemic stroke, PFKFB3 inhibitor alleviates motor discoordination and brain infarct injury [16]