Complement activation participates in tissue injury after temporary loss of blood flow (ischemia-reperfusion injury). Recently reported evidence indicates that complement activation is a pathologic mechanism of injury in the post-hypoxic-ischemic neonatal brain. Therefore, recently developed complement inhibitors may find a role in the amelioration of neonatal hypoxic-ischemic cerebral injury. Further research is needed to better define the role of complement in human neonatal cerebral injury and to determine the neuroprotective effect and safety of pharmacologic agents designed to inhibit complement.
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