Brain arteriovenous malformations (BAVM) have high matrix metalloproteinase-9 (MMP-9) expression, the source of which is unclear. We hypothesized MMP-9 production might be due to inflammation in BAVM. Compared to control brain tissues (n = 5), BAVM tissue (n = 139) had a higher expression (by ELISA) of myeloperoxidase (MPO) (193 +/- 189 vs. 6 +/- 3, ng/mg, P < .001), MMP-9 (28 +/- 32 vs. 0.7 +/- 0.6, ng/mg, P < .001), and IL-6 (102 +/- 218 vs. 0.1 +/- 0.1, pg/mg, P < .001), but not eNOS (114 +/- 87 vs. 65 +/- 9, pg/mg, P = .09). MMP-9 expression in BAVM highly correlated with myeloperoxidase (R2 = .76, P < .001), as well as with IL-6 (R2 = .32, P < .001). In contrast, MMP-9 in BAVM poorly correlated with the endothelial marker, eNOS (R2 = .03, P = .05), and CD31 (R2 = .004, P = .57). Compared to non-embolized patients (n = 46), patients with pre-operative embolization (n = 93) had higher levels of myeloperoxidase (236 +/- 205 vs. 106 +/- 108, ng/mg, P < .001) and MMP-9 (33 +/- 35 vs. 16 +/- 20, ng/mg, P < .001), however the correlation between MMP-9 and myeloperoxidase was equally strong for both groups (R2 = .69, n = 93, P < .001, for both). MMP-9 expression correlated with the lipocalin-MMP-9 complex, suggesting neutrophils as the MMP-9 source. MPO co-localized with majority of MMP-9 signal by immunohistochemistry. Our data suggest that inflammation is a prominent feature of BAVM lesional phenotype, and neutrophils appear to be a major source of MMP-9 in these lesions.
Vasospasm that occurs after subarachnoid hemorrhage (SAH), despite successful surgical or radiological intervention remains with an ominous prognostic recovery period. 1 We investigated the correlation of S100B protein in CSF and serum with incident of vasospasm and neurological outcome in patients undergoing intracerebral aneurysm clipping. Twenty five patients were enrolled. All patients received combined anesthetic techniques. Brain protection was provided by isoflurane. A CSF sample (2 cc) and blood sample (5 cc) were drawn 3 times (before skin incision, 30 minutes and 24 hours after clipping). Patients were followed for the incidence of vasospasm in Neurosurgical Intensive Care Unit and the neurological status at discharged was assessed using Glasgow Outcome Scale. Compared with baseline level (at 0 minute) we found that early changes in CSF S100 B level at 30 minutes significantly correlate with vasospasm (P = 0.005, sensitivity 90% and specificity 90%) but the correlation dissipated at 24 hours. In addition, early changes in S100B in CSF at 30 minutes significantly correlate with neurological outcome (P = 0.003). The relationship persisted at 24 hours (P , 0.011). In Serum we found no significant correlation between S100B at 30 minutes or 24 hours with either vasospasm or neurological outcome. We conclude that changes of S100B level in CSF in patients undergoing intracerebral aneurysm clipping surgery are strongly correlated with vasospasm and can be a reliable diagnostic tool to identified patients who are endangered with evolving vasospasm after a successful securing aneurysm surgery. Reference: 1. Pluta RM. Delayed cerebral vasospasm and nitric oxide: review, new hypothesid, and proposed treatment.
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