Inflammatory Response of the Brain Following Cerebral Ischemia

摘要

Brain injury following cerebral ischemia develops from a complex series of pathophysiological events. Ischemia due to middle cerebral artery occlusion encompasses a densely ischemic focus and a less densely ischemic penumbral zone. Cells in the penumbra may be salvaged by reperfusion or by drugs that prevent an extension of the infarction into the penumbral zone. Factors responsible for such an extension include acidosis, edema formation, acute local inflammation, dissipative ion fluxes, calcium overload, glutamate excitotoxicity, free radical formation, nitric oxide overproduction and programmed cell death. There is increasing evidence that ischemic brain injury secondary to arterial occlusion is characterized by acute local inflammation, which involves accumulation of polymorphonuclear neutrophils (PMN). Factors that influence the recruitment of PMN could represent new therapeutic targets in acute stroke. Overexpression of inflammatory mediators such as cytokines, chemokines and adhesion molecules promotes recruitment of leukocytes in the ischemic area.