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https://hdl.handle.net/2440/27212
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Type: | Conference paper |
Title: | Increased substance P immunoreactivity and edema formation following reversible ischemic stroke |
Author: | Turner, R. Blumbergs, P. Sims, N. Helps, S. Rodgers, K. Vink, R. |
Citation: | Acta Neurochirurgica: Supplementum, 2006 / Hoff, J., Keep, R., Xi, G., Hua, Y. (ed./s), vol.96, iss.96, pp.263-266 |
Publisher: | Springer-Verlag |
Publisher Place: | New York |
Issue Date: | 2006 |
Series/Report no.: | Acta Neurochirurgica Supplementum |
ISBN: | 3211307125 9783211307120 |
ISSN: | 0065-1419 |
Conference Name: | Acta Neurochirurgica Supplement 96 (1 Jun 2005 - 3 Jun 2005 : Michigan, USA) |
Editor: | Hoff, J. Keep, R. Xi, G. Hua, Y. |
Statement of Responsibility: | by R.J. Turner, P.C. Blumbergs, N.R. Sims, S.C. Helps, K.M. Rodgers and R. Vink |
Abstract: | Previous results from our laboratory have shown that neurogenic inflammation is associated with edema formation after traumatic brain injury (TBI). This neurogenic inflammation was characterized by increased substance P (SP) immunoreactivity and could be attenuated with administration of SP antagonists with a resultant decrease in edema formation. Few studies have examined whether neurogenic inflammation, as identified by increased SP immunoreactivity, occurs after stroke and its potential role in edema formation. The present study examines SP immunoreactivity and edema formation following stroke. Experimental stroke was induced in halothane anaesthetized male Sprague-Dawley rats using a reversible thread model of middle cerebral artery occlusion. Increased SP immunoreactivity at 24 hours relative to the non-infarcted hemisphere was observed in perivascular, neuronal, and glial tissue, and within the penumbra of the infarcted hemisphere. It was not as apparent in the infarct core. This increased SP immunoreactivity was associated with edema formation. We conclude that neurogenic inflammation, as reflected by increased SP immunoreactivity, occurs following experimental stroke, and that this may be associated with edema formation. As such, inhibition of neurogenic inflammation may represent a novel therapeutic target for the treatment of edema following reversible, ischemic stroke. |
Keywords: | Cerebral Cortex Animals Rats Rats, Sprague-Dawley Brain Edema Reperfusion Injury Substance P Inflammation Mediators Male Stroke |
DOI: | 10.1007/3-211-30714-1_56 |
Published version: | http://dx.doi.org/10.1007/3-211-30714-1_56 |
Appears in Collections: | Aurora harvest 2 Medicine publications |
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