Complement inhibition does not reduce post-hypoxic-ischemic cerebral injury in 21-day-old rats.

Hypoxic-ischemic (HI) cerebral injury frequently follows resuscitation and is a recognized cause of permanent long-term neurologic disability in children. Complement activation has been shown to participate in post-ischemic injury to a variety of tissues and organs. To test the hypothesis that complement activation participates in post-HI cerebral injury in immature rats, 21-day-old rats were subjected to right common carotid artery ligation and 8% O(2). This combination of ischemia and hypoxia resulted in the development of significant neuronal loss, edema, and atrophy in the right cerebral hemisphere. However, intraperitoneal administration of the complement inhibitors soluble complement receptor type 1 or cobra venom factor did not reduce the neuronal loss, edema, or atrophy. Therefore, complement activation did not contribute significantly to the cerebral injury observed in this immature rat model.