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https://hdl.handle.net/2440/5751
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dc.contributor.author | Vink, R. | - |
dc.contributor.author | Donkin, J. | - |
dc.contributor.author | Cruz, M. | - |
dc.contributor.author | Nimmo, A. | - |
dc.contributor.author | Cernak, I. | - |
dc.date.issued | 2004 | - |
dc.identifier.citation | Journal of the American College of Nutrition, 2004; 23(5):538S-540S | - |
dc.identifier.issn | 0731-5724 | - |
dc.identifier.issn | 1541-1087 | - |
dc.identifier.uri | http://hdl.handle.net/2440/5751 | - |
dc.description.abstract | Objective: Magnesium (Mg) deficiency has been shown to increase substance P release and induce a pro-inflammatory response that can be attenuated with the administration of a substance P-antagonist. Neurogenic inflammation has also been implicated in traumatic brain injury (TBI), a condition where brain intracellular free magnesium (Mgf) decline is known to occur and has been correlated with functional outcome. We therefore examined whether a substance P antagonist restores brain intracellular free magnesium concentration following TBI. Methods: Male, adult Sprague-Dawley rats were injured using the Cernak impact acceleration model of diffuse TBI. At 30 min after injury, animals were administered either 0.25 mg/kg i.v. n-acetyl tryptophan or equal volume saline. Prior to and 4 h after induction of injury, phosphorus magnetic resonance spectra were acquired using a 7-tesla magnet interfaced with a Bruker console. Mgf was calculated from the chemical shift of the beta ATP. Before injury, Mgf was 0.51 ± 0.05 mM (SEM). Results: By 4 hr after injury, Mgf had significantly declined to 0.27 ± 0.02 mM in saline treated rats. In contrast, rats treated with n-acetyl tryptophan had a Mgf of 0.47 ± 0.06 mM at 4 h after injury, which was not significantly different from preinjury values. There were no significant differences in pH between the treatment groups. Conclusion: It seems that any beneficial effect of a substance P antagonist on functional outcome following TBI may be related to improvement in brain Mg homeostasis induced by the compound. | - |
dc.description.statementofresponsibility | Robert Vink, J. J. Donkin, M. I. Cruz, Alan J Nimmo, and Ibolja Cernak | - |
dc.language.iso | en | - |
dc.publisher | Amer Coll Nutrition | - |
dc.rights | Copyright © 2004 by the American College of Nutrition | - |
dc.source.uri | http://www.jacn.org/cgi/content/full/23/5/538S | - |
dc.subject | brain trauma | - |
dc.subject | brain Mg | - |
dc.subject | inflammation | - |
dc.subject | functional outcome | - |
dc.subject | rats | - |
dc.subject | substance P-antagonist | - |
dc.title | A substance P antagonist increases brain intracellular free magnesium concentration after diffuse traumatic brain injury in rats | - |
dc.type | Journal article | - |
dc.identifier.doi | 10.1080/07315724.2004.10719398 | - |
pubs.publication-status | Published | - |
dc.identifier.orcid | Vink, R. [0000-0002-4885-0667] | - |
Appears in Collections: | Aurora harvest Pathology publications |
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