RESUMO
To determine whether ischemic cerebral infarction is mediated in part by complement component C9, C9-deficient neonatal rats were subjected to unilateral cerebral ischemia. Brains were harvested 24 h later, stained with 2,3,5-triphenyl tetrazolium chloride, and cerebral infarct volumes were quantified by computer-based planimetry. Compared with buffer, prophylactic intraperitoneal (i.p.) administration of the complement inhibitors soluble complement receptor type 1 (sCR1), a molecular hybrid of sCR1 and the selectin inhibitor sialyl Lewis x (sCR1-sLex), or cobra venom factor did not affect the cerebral infarct volume. In contrast, i.p. human C9 (75 microg/g body weight) significantly increased the volume of infarct located 6 through 10 mm posterior to the frontal pole. Therefore, in the post-ischemic brain, C9 was neurotoxic and augmented the focal cerebral infarct volume.
