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The pathogenesis of brain damage from cerebrovascular occlusion may be separated into two sequential processes:(a)vascular and haematological events that cause the initial reduction and subsequent alteration of local cerebral blood flow;and(b)ischaemia-induced abnormalities of cellular chemistry that produce necrosis of neurons,glia,and other supportive brain cells.In this article I will summarise important mechanisms of cellular necrosis.The molecular consequences of brain ischaemia include changes in cell signaling(neurotransmitters,neuromodulators);in signal transduction (receptors,ion channels,second messengers,phosphorylation reactions);in metabolism(carbohydrate,protein,fatty acid,free radicals);and in gene regulation/expression.Investigators who seek to ameliorate or prevent stroke damage must distinguish reversible changes that cause only cellular dysfunction from processes that cause irreversible injury.Moreover,despite a common ischaemic insult,different mechanisms underlie necrosis of neurons and flia,and probably even necrosis of distinct neuronal types. |
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