Reperfusion injury:
Restoration of blood flow to ischemic tissues can promote recovery of cells if they are reversibly injured, but can also paradoxically exacerbate the injury and cause cell death.
Mechanism:
The likely answer is that new damaging processes are set in motion during reperfusion, causing the death of cells that might have recovered otherwise. Several mechanisms have been proposed.
- Oxidative stress. New damage may be initiated during reoxygenation by increased generation of reactive oxygen and nitrogen species.
- Intracellular calcium overload. Intracellular and mitochondrial calcium overload begins during acute ischemia; it is exacerbated during reperfusion due to influx of calcium resulting from cell membrane damage and ROS mediated injury to sarcoplasmic reticulum.
- Inflammation. Ischemic injury is associated with inflammation as a result of “dangers signals” released from dead cells, cytokines secreted by resident immune cells such as macrophages, and increased expression of adhesion molecules by hypoxic parenchymal and endothelial cells, all of which act to recruit circulating neutrophils to reperfused tissue.
- Activation of the complement system may contribute to ischemia-reperfusion injury.
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