Excitotoxicity and Oxidative Stress in Acute Ischemic Stroke

Abstract

The term “stroke” is applied to a heterogeneous group of diseases caused by decreased perfusion of the brain due to occlusion of the blood vessels supplying the brain or a haemorrhage originating in them. Most strokes (~ 85%) are ischemic; that is, they result from occlusion of a major cerebral artery by a thrombus or embolism. This results in reduced blood flow and a major decrease in the supply of oxygen and nutrients to the affected region. The rest of strokes are haemorrhagic: caused by the rupture of a blood vessel either in the brain or on its surface. Strokes deprive the brain not only of oxygen but also of glucose and of all other nutrients, as well as disrupting the nutrient/waste exchange process required to support brain metabolism. The result is the development of a hypoxic-ischemic state. Ischemia is defined as a decrease in blood flow to tissues that prevents adequate delivery of oxygen, glucose and others nutrients. Ischemic stroke is the result of total or partial interruption of cerebral arterial blood supply, which leads to oxygen and glucose deprivation of the tissue (ischemia). If cerebral arterial blood flow is not restored within a short period, cerebral ischemia is the usual result, with subsequent neuron death within the perfusion territory of the vessels affected. Ischemic stroke is characterized by a complex sequence of events that evolves over hours or even days [1-3]. Acute ischemic stroke results from acute occlusion of cerebral arteries. Cerebral ischemia occurs when blood flow to the brain decreases to a level where the metabolic needs of the tissue are not met. Cerebral ischemia may be either transient (followed by reperfusion) or essentially permanent. In all cases, a stroke involves dysfunction and death of brain neurons and neurological damage that reflects the location and size of the brain area affected.