Abstract
The occlusion of a cerebral artery by a thrombus accounts for about 80% of strokes. Reperfusion can save hypoperfused brain tissue from early cerebral blood flow restoration (CBF), thus limiting neurological impairment. The most successful treatments for stroke care have proven to be reperfusion techniques. One of the key drawbacks of these treatment methods is that early ischemic brain tissue reperfusion can lead to adverse effects, including blood-brain barrier breakdown, which can lead to cerebral oedema, haemorrhage of the brain, or both. Haemorrhages are especially devastating after reperfusion and are associated with exceptionally high morbidity and mortality. Fear of haemorrhage-related reperfusion greatly restricts the use of stroke therapies. Reperfusion injury, a mechanism that further damages brain cells, the ischemic arterial wall, and the microvasculature, is due to the deleterious effects of early restoration of cerebral blood flow following stroke. It seems clear that the brain will benefit from therapies to restore CBF to an ischemic region. The brain's reliance on normal CBF levels is underlined by the sensitivity of the brain to relatively short ischaemic cycles. Experimental and clinical data, however, suggests that tissue damage can be aggravated by organ reperfusion. [1] Studies have failed to prove that infarct size is increased by reperfusion. Reperfusion can aggravate the formation of oedema and lead to abnormal blood flow patterns and microvascular lesions within the reperfused areas.
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