No apparent role for neutrophils and neutrophil-derived myeloperoxidase in experimental subarachnoid haemorrhage and vasospasm: a preliminary study.

Abstract

The literature contains investigations and discussion of the role of neutrophils and neutrophil-derived myeloperoxidase (MPO) in inflammatory processes, local ischaemia, and ischaemia-reperfusion injury models. Our aim was to determine whether the same roles existed for neutrophils and the system involving neutrophil-derived MPO in experimental subarachnoid haemorrhage (SAH) and associated ischaemia. Forty-eight adult New Zealand white rabbits were divided into six groups of eight. The first SAH model was applied to 16 animals. Eight of these rabbits were sacrificed after 48 hours (Group 1) and the remaining eight were killed after 96 hours (Group 2). The second SAH model applied to another 16 rabbits, which were sacrificed in two groups at the above time periods, forming Groups 3 and 4, respectively. There were two groups of 8 control animals, one group per SAH model, and these rabbits were sacrificed after 48 hours. We carried out histopathological studies using haematoxylin and eosin (H&E) stain, elastin stain, MPO immunohistochemistry, and determination of basilar artery cross-sectional diameter. We also did biochemical 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. In contrast to previous experimental findings in local ischaemia and ischaemia-reperfusion models, we found no histopathological or biochemical evidence to suggest a role for neutrophils and neutrophil-derived MPO in relation to subarachnoid haemorrhage and resultant vasospasm. Although we confirmed the successful induction of significant vasospasm and observed the clinical evidences of subsequent ischaemia, there was no notable accumulation of neutrophils or activity of neutrophil-derived MPO in the tissues studied. This suggests that the biological process induced by SAH follows a different pattern from that seen in local ischaemia and ischaemia-reperfusion injury.