A substance P antagonist increases brain intracellular free magnesium concentration after diffuse traumatic brain injury in rats
Vink, Robert, Donkin, J.J., Cruz, M.I., Nimmo, Alan J., and Cernak, Ibolja (2004) A substance P antagonist increases brain intracellular free magnesium concentration after diffuse traumatic brain injury in rats. Journal of the American College of Nutrition, 23 (5). 538S-540S.
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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.
|Item Type:||Article (Refereed Research - C1)|
|Keywords:||brain Mg; brain trauma; functional outcome; inflammation; rats; substance P-antagonist|
|Date Deposited:||23 Mar 2010 22:49|
|FoR Codes:||11 MEDICAL AND HEALTH SCIENCES > 1109 Neurosciences > 110999 Neurosciences not elsewhere classified @ 100%|
|SEO Codes:||92 HEALTH > 9299 Other Health > 929999 Health not elsewhere classified @ 100%|
|Citation Count from Web of Science||