Neuroprotective efficacy of magnesium sulphate in experimental traumatic brain injury

Objective

Traumatic brain injury (TBI) results in brain damage either by early cell death or by delayed cell death due to secondary injury factors such as blood–brain barrier breakdown, brain edema, and cerebral ischemia. Studies have demonstrated that magnesium (Mg) salts given after traumatic brain injury improve neurological outcome. We aimed to examine the neuroprotective effects of magnesium on brain edema and blood–brain barrier breakdown after experimental traumatic brain injury in rats.

Method

Experimental closed head trauma was induced on Sprague-Dawley rats by allowing 450 g weight falling from a 2 m height onto a metallic disc fixed to the intact skull. The animals were randomly assigned to receive an intraperitoneal bolus of either 750 μmol/kg magnesium sulphate or 1 ml saline 30 min after the induction of TBI. Brain water content (BWC) and brain tissue specific gravity (SG), as indicators of brain edema, were measured 24 hours after traumatic brain injury. Blood–brain barrier integrity was evaluated quantitatively 24 hours after injury by fluorometric assay of Evans Blue dye (EBD) extravasations.

Results

In magnesium group, brain tissue specific gravity was significantly increased and brain water content was significantly reduced. Evans blue dye content in the brain tissue was significantly decreased in the magnesium group (Table 1).

Table 1 Brain water content, specific gravity and Evans blue dye content in the brain tissue

Conclusion

These experimental results have demonstrated the neuroprotective effects of magnesium sulphate on secondary injury factors like brain edema and blood–brain barrier breakdown after traumatic brain injury.