ANTICARDIOLIPIN ANTIBODY AGGRAVATES CEREBRAL VASOSPASM AFTER SUBARACHNOID HEMORRHAGE IN RABBITS

Background and Purpose-We previously reported that patients with antip hospholipid antibodies (aPLs) frequently demonstrate cerebral infarcti on due to cerebral vasospasm after subarachnoid hemorrhage (SAH). To e xamine the participation of aPLs in the pathogenesis of vasospasm afte r SAH, we studied the relationships of aPLs and SAH in an animal model . Methods-SAH was produced in 34 rabbits that received two subarachnoi d injections of autologous arterial blood. The animals were divided in to four experimental groups: SAH was induced in group A (n=9), intracu taneous injection of cardiolipin (CL) was performed before the inducti on of SAH in group B (n=5), intravenous injection of CL was performed before SAH in group C (n=12), and cyclosporin A was infused intravenou sly after the intravenous injection of CL and induction of SAH in grou p D (n=8). Enzyme-Linked immunosorbent assay identifying the titer of IgG CL antibodies, neurological evaluation, cerebral angiography, and histological examination were performed in all four groups. Results-A significant elevation of anti-CL antibodies, aggravation of neurologic al deficit, and reduction of caliber of the basilar artery were observ ed in rabbits that received the intravenous immunization of CL (group C). The administration of cyclosporin A reduced the titer of anti-CL a ntibody, aggravation of neurological deficit, constriction of basilar artery, and the incidence of cerebral infarction (group D). Conclusion s-Anti-CL antibodies may therefore be involved in the deterioration of cerebral vasospasm after SAH.