The pathophysiology of ischemic brain injury

Brain tissue ischemia and hypoxia may be due to a variety of mechanisms to activate the Erzhi brain edema and neuronal injury, and the resulting patient permanent disability and even death. Cerebral ischemia and hypoxia, microcirculation and cerebral ischemia after free radicals, arachidonic acid metabolites, excitatory amino acids and free fatty acids increased, resulting in severe vasogenic and cell-derived brain edema. Cerebral blood flow, vascular endothelial hypoxic injury and permeability increased destruction of blood-brain barrier function, resulting in secondary brain edema occurs when blood flow recanalization. The cerebral edema cerebral perfusion pressure changes and the enormous changes of the extracellular environment and further increase the brain tissue ischemia and hypoxia, and secondary apoptosis and inflammatory responses, forming a vicious cycle until the cell death.

In the middle cerebral artery occlusion and reperfusion (MCAO melon) model, starting with the glutamate-dependent, excitotoxic nerve damage. Hours is followed by cell death stage of infarct development to peripheral areas and the cerebral cortex when neuronal injury and apoptosis and inflammatory responses. Ischemia-induced neuronal damage response includes the following three mechanisms: ischemia-induced expression of IL-1pmRNA; ischemia-induced neuronal apoptosis; ischemia-induced glial reaction. Exacerbate neuronal death caused by the mechanism of apoptosis in the early stages of cell death caused by inflammation. Interleukin-1 (inierlukin a 1, IL-1) is the inflammation of early cytokines, is considered to be important factors controlling neuronal apoptosis induced by ischemic brain injury. One result of ischemia-mediated inflammatory response is the activation and infiltration of mononuclear cells, the cerebral cortex of macrophages / microglia infiltration and activation is a characteristic reaction of ischemic stroke-induced inflammation. Can be found in a large number of macrophages / microglia in the infarcted cerebral hemisphere contralateral but not MCAO rat brain cortex around the infarct area after 24h of glial fibrillary acidic protein (gelatinousfiberac remember Protein GEAp) immune response was significantly enhanced, suggesting the presence of astrocytes.


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