2002
DOI: 10.3171/jns.2002.97.3.0537
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Rise in serum soluble intercellular adhesion molecule—1 levels with vasospasm following aneurysmal subarachnoid hemorrhage

Abstract: These data suggest a role for ICAM-1 in the pathophysiology of cerebral vasospasm or its ischemic sequelae. As this relationship is further elucidated, adhesion molecules such as ICAM-1 may provide novel therapeutic targets in the prevention of vasospasm or its ischemic consequences.

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Cited by 60 publications
(44 citation statements)
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“…The occurrence of DIND (ischemic lesion in the CT scan) did not correlate with the values of both adhesion molecules in our study. But the increase in blood flow velocity in the TCD sonography correlated statistically significant to a secondary increase in adhesion molecules in the CSF and serum similar to the study conducted by Mocco et al [31]. However one has to be very careful to interpret TCD data because flow velocities do not necessary represent cerebral blood flow.…”
Section: Discussionsupporting
confidence: 49%
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“…The occurrence of DIND (ischemic lesion in the CT scan) did not correlate with the values of both adhesion molecules in our study. But the increase in blood flow velocity in the TCD sonography correlated statistically significant to a secondary increase in adhesion molecules in the CSF and serum similar to the study conducted by Mocco et al [31]. However one has to be very careful to interpret TCD data because flow velocities do not necessary represent cerebral blood flow.…”
Section: Discussionsupporting
confidence: 49%
“…Mocco et al [31] studied 89 patients suffering from aneurysmal SAH. Levels of soluble ICAM-1 were determined in blood samples using an enzyme-linked immunosorbent assay every other day for 12 days after SAH.…”
Section: Discussionmentioning
confidence: 99%
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“…Its exact pathophysiologic mechanisms are not fully established and multi-factorial processes that contain oxygen free radicals, endothelin, vascular endothelial growth factor, arachidonic acid derivatives, lipid peroxidation, inactivation of nitrous oxide (NO), activation of protein kinase C system released from blood clots in the subarachnoid spaces and cisterns, are known to be related to cerebral vasospasm 3,10,12,14,15,19,21,22,24,31,[35][36][37] . There are numerous clinical studies that early surgical removal of blood clots and massive irrigation may reduce the risk of cerebral vasospasm 13,18,23) .…”
Section: Discussionmentioning
confidence: 99%
“…Inflammatory mediators, such as interleukin-6, tumor necrosis factor, intracellular adhesion molecule, matrix metalloproteinase 9, and C-reactive protein, have been linked to DCI and are downregulated through preconditioning. [40][41][42][43][48][49][50][51][52][53][54] In addition, tissue is rendered more tolerant to ischemia through reduction of excitotoxicity and metabolic protection by enhancing mitochondrial function. Preconditioning also affects several other pathways that have been implicated in vasospasm and DCI.…”
Section: Preconditioning To Ameliorate Vasospasm and DCImentioning
confidence: 99%