Nonenzymatic derived lipid peroxide, 8-iso-PGF2α, participates in the pathogenesis of delayed cerebral vasospasm in a canine SAH model

Abstract

We studied whether 8-iso-PGF2α, nonenzymatic arachidonyl peroxide, participated in the pathogenesis of delayed vasospasm using a canine subarachnoid hemorrhage (SAH) model. Fourteen adult mongrel dogs were divided into two groups, two-hemorrhage SAH group (n = 8) and control group (n = 6). The contents of 8-iso-PGF 2α in CSF, the basilar artery segment, and subarachnoid clot were measured by enzyme immunoassay kit. The CSF 8-iso-PGF2α content on Day 7 in the SAH group was 67.9 ± 29.9 pg ml-1 (n = 8), which was significantly higher than 27.1 ± 13.8 (n = 8) on Day 0 in the SAH group, and 33.2 ± 14.4 pg ml-1 (n = 5) on Day 7 in the control group. The 8-iso-PGF2α content in the basilar artery segment with spasm on Day 7 in the SAH group was 13.5 ± 1.9 pg mg-1 wet weight (n = 8), significantly higher than 8.7 ± 1.9 (n = 6) in the control group. The 8-iso-PGF2α content in subarachnoid clot was 1.7 ± 1.4 ng g-1 wet weight (n = 8). Significant elevation of the 8-iso-PGF2α contents in the CSF and the basilar artery segment occurred on Day 7 in the SAH group. The subarachnoid clot enclosed the basilar artery on Day 7, contained a considerable amount of 8-iso-PGF2α. These results suggested that 8-iso-PGF2α could play a crucial role in the pathogenesis of the delayed cerebral vasospasm. [Neurol Res 2002; 24: 301-306]