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 (Mg2+) and total
magnesium concentrations that is significantly correlated with the severity of injury. In order to further investigate the relationship between Mg2+ and
brain injury, we examined the effect of Mg2+ treatment on posttraumatic neurological outcome following fluid-percussion
brain injury (2.0 atm) in rats. Since administration of
ATP-MgCl2 has been shown to be beneficial in a variety of models of organ
ischemia, we also examined the efficacy of
ATP-MgCl2 or
ATP alone in the treatment of experimental
brain injury. Animals treated with low (12.5 mumol) or high (125 mumol) dose
MgCl2 at 30 min postinjury showed a significant dose-dependent improvement in neurological function when compared to saline-treated controls. Treatment with
ATP-MgCl2 (12.5 mumol) or
ATP alone (12.5 mumol) caused no significant improvement in chronic neurological outcome. MgCl2-treated animals showed no change in postinjury mean arterial blood pressure (MAP), whereas animals treated with either
ATP-MgCl2 or
ATP alone showed a transient but significant fall in MAP (P less than 0.01) during the
drug-infusion period. Our results suggest that postinjury treatment with
MgCl2 is effective in limiting the extent of neurological dysfunction following experimental
traumatic brain injury in the rat.