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A substance P antagonist increases brain intracellular free magnesium concentration after diffuse traumatic brain injury in rats
Journal article   Peer reviewed

A substance P antagonist increases brain intracellular free magnesium concentration after diffuse traumatic brain injury in rats

R Vink, James J Donkin, M I Cruz, A J Nimmo and I Cernak
Journal of the American College of Nutrition, Vol.23(5), pp.538S-540S
2004
DOI: https://doi.org/10.1080/07315724.2004.10719398
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https://doi.org/10.1080/07315724.2004.10719398View
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Abstract

brain trauma substance P-antagonist rats functional outcome inflammation brain Mg
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.

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