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Cerebrovascular injury in stroke

Stroke is a major cause of morbidity and mortality across all industrialized countries with the most common form of stroke being ischemic stroke. The pathophysiology of ischemic stroke involves the occlusion of a vessel on the arterial side of the cerebral circulation. Specifically, the middle cerebral artery (MCA) is the most common site of occlusion, accounting for y75% of all ischemic strokes. Owing to the severe sensitivity that brain cells have to anoxic environments, neuronal death occurs quickly in the setting of severe ischemia. Given the pathophysiology of ischemic stroke, it is logical that its successful treatment should involve the early reestablishment of tissue perfusion. Indeed, techniques for reperfusion of ischemic areas of the brain have been developed, and more promising techniques continue to be developed. However, the reperfusion of ischemic brain brings with it the price of reperfusion damage, if the reperfusion is not initiated in acute chronologic proximity to the onset of ischemia. The damage that occurs owing to reperfusion injury ranges across a broad spectrum of severity, from minor reversible damage to severe irreversible damage that can cause neurological deficits or death. On the cellular level, the onset of anoxia in ischemic brain initiates a cascade of intracellular events within affected cells, which eventually leads to the death of the cells. One of the crucial intracellular events that leads to cellular death is the massive increase in intracellular calcium concentration ([Ca]in), which activates Ca-dependent hydrolytic enzymes, leading to the formation of reactive oxygen species and causing increases in cytokine production, as well as up-regulation of molecular adhesive molecules that directly mediate inflammatory injury to cells. During the acute onset of reperfusion, the reestablishment of adequate blood flow and oxygen supply to the damaged area of brain exacerbates tissue destruction by intensifying the accumulation of blood-borne inflammatory cells, microvascular dysfunction and overproduction of oxygen free radicals that is associated with lipid peroxidation.