No apparent role for neutrophils and neutrophil-derived myeloperoxidase inexperimental subarachnoid haemorrhage and vasospasm: A preliminary study

Objective. The literature contains investigations and discussion of the rol e of neutrophils and neutrophil-derived myeloperoxidase (MPO) in inflammato ry processes, local ischaemia, and ischaemia-reperfusion injury models. Our aim was to determine whether the same roles existed for neutrophils and th e system involving neutrophil-derived MPO in experimental subarachnoid haem orrhage (SAH) and associated ischaemia. Material and Method. Forty-eight adult New Zealand white rabbits were divid ed into six groups of eight. The first SAM model was applied to 16 animals. Eight of these rabbits were sacrificed after 48 hours (Group 1) and the re maining eight were killed after 96 hours (Group 2). The second SAM model ap plied to another 16 rabbits, which were sacrificed in two groups at the abo ve time periods, forming Groups 3 and 4, respectively. There were two group s of 8 control animals, one group per SAM model, and these rabbits were sac rificed after 48 hours. We carried out histopathological studies using haem atoxylin and eosin (H&E) stain, elastin stain, MPO immunohistochemistry, an d determination of basilar artery cross-sectional diameter. We also did bio chemical analysis of cerebral hemisphere and brainstem specimens, measuring tissue lipid peroxidase and MPO activity. Results were compared between the groups and with their related controls. R esults. In contrast to previous experimental findings in local ischaemia an d ischaemia-reperfusion models, we found no histopathological or biochemica l evidence to suggest a role for neutrophils and neutrophil-derived MPO in relation to subarachnoid haemorrhage and resultant vasospasm. Although we c onfirmed the successful induction of significant vasospasm and observed the clinical evidences of subsequent ischaemia, there was no notable accumulat ion of neutrophils or activity of neutrophil-derived MPO in the tissues stu died. This suggests that the biological process induced by SAH follows a di fferent pattern from that seen in local ischaemia and ischaemia-reperfusion injury.