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Magnesium protects against neurological deficit after brain injury
T K McIntosh1, R Vink, I Yamakami
1Department of Surgery, University of Connecticut Health Center, Farmington 06032.
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 (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.
Insights
Magnesium (Mg2+) treatment after brain injury in rats improved neurological function. This study suggests Mg2+ may limit neurological damage following traumatic brain injury.
Area of Science:
- Neuroscience
- Biochemistry
- Traumatology
Background:
- Secondary damage to the central nervous system (CNS) after injury involves speculative biochemical factors.
- Brain injury in rats is associated with a significant decline in intracellular and total magnesium (Mg2+) concentrations, correlating with injury severity.
Purpose of the Study:
- To investigate the effect of Mg2+ treatment on neurological outcomes after experimental brain injury.
- To evaluate the efficacy of ATP-MgCl2 and ATP alone in treating experimental brain injury.
Main Methods:
- Rats with fluid-percussion brain injury received MgCl2, ATP-MgCl2, or ATP alone 30 minutes postinjury.
- Neurological function and mean arterial blood pressure (MAP) were monitored.
Main Results:
- MgCl2 treatment (12.5 or 125 mumol) resulted in a dose-dependent improvement in neurological function compared to saline controls.
- ATP-MgCl2 or ATP alone did not significantly improve chronic neurological outcomes.
- MgCl2 treatment did not alter MAP, while ATP-MgCl2 and ATP caused a transient MAP decrease.
Conclusions:
- Postinjury administration of MgCl2 is effective in mitigating neurological dysfunction after experimental traumatic brain injury in rats.
- Mg2+ treatment appears to be a promising therapeutic strategy for traumatic brain injury, without adverse effects on blood pressure.