Magnesium protects against neurological deficit after brain injury

Abstract

The biochemical factors that mediate secondary or delayed damage to the central nervous system (CNS) remain speculative. We have recently demonstrated that brain injury in rats causes a rapid decline in brain intracellular free magnesium (Mg 2+) and total magnesium concentrations that is significantly correlated with the severity of injury. In order to further investigate the relationship between Mg 2+ and brain injury, we examined the effect of Mg 2+ treatment on posttraumatic neurological outcome following fluid-percussion brain injury (2.0 atm) in rats. Since administration of ATP-MgCl 2 has been shown to be beneficial in a variety of models of organ ischemia, we also examined the efficacy of ATP-MgCl 2 or ATP alone in the treatment of experimental brain injury. Animals treated with low (12.5 μmol) or high (125 μmol) dose MgCl 2 at 30 min postinjury showed a significant dose-dependent improvement in neurological function when compared to saline-treated controls. Treatment with ATP-MgCl 2 (12.5 μmol) or ATP alone (12.5 μmol) caused no significant improvement in chronic neurological outcome. MgCl 2-treated animals showed no change in postinjury mean arterial blood pressure (MAP), whereas animals treated with either ATP-MgCl 2 or ATP alone showed a transient but significant fall in MAP ( P<0.01) during the drug-infusion period. Our results suggest that postinjury treatment with MgCl 2 is effective in limiting the extent of neurological dysfunction following experimental traumatic brain injury in the rat.