Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/5751
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Type: Journal article
Title: A substance P antagonist increases brain intracellular free magnesium concentration after diffuse traumatic brain injury in rats
Author: Vink, R.
Donkin, J.
Cruz, M.
Nimmo, A.
Cernak, I.
Citation: Journal of the American College of Nutrition, 2004; 23(5):538S-540S
Publisher: Amer Coll Nutrition
Issue Date: 2004
ISSN: 0731-5724
1541-1087
Statement of
Responsibility: 
Robert Vink, J. J. Donkin, M. I. Cruz, Alan J Nimmo, and Ibolja Cernak
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.
Keywords: brain trauma; brain Mg; inflammation; functional outcome; rats; substance P-antagonist
Rights: Copyright © 2004 by the American College of Nutrition
RMID: 0020041481
DOI: 10.1080/07315724.2004.10719398
Published version: http://www.jacn.org/cgi/content/full/23/5/538S
Appears in Collections:Pathology publications

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