Neuroprotective effects of preischemia subcutaneous magnesium sulfate in transient cerebral ischemia

Objective: Neurological injury due to transient cerebral ischemia is a potential complication of cardiovascular surgery. The neuroprotective effect of magnesium, when given subcutaneously before the ischemia, was assessed in a rat model of transient global cerebral ischemia. Methods: Thirty-six male Wistar albino rats were included to this randomized, controlled, prospective study. In 24 animals, ischemia was induced with four-vessel occlusion technique with the duration of 15 min. MgSO4 was given 600 mg/kg subcutaneously 48 h before the procedure in group 1 (n = 12). Similar volume of saline solution was used in animals of control group (group 2, n = 12). The animals in group 3 (sham group, n = 12) were anesthetized and subjected to operative dissections without vascular occlusion. Physiological parameters and somatosensory evoked-potentials (SEP) were monitored in animals before ischemia, during ischemia and in the first 30 min of reperfusion. Their neurological outcome had been clinically evaluated and scored up to 4 days postischemia. The intergroup differences were compared. Then the animals were sacrificed and their brains were processed for histopathological examination. Results: In group 3, SEP amplitudes did not change during the procedures, and all animals recovered without neurologic deficits. At the end of ischemic period, the average amplitude was reduced to 5 ± 3% of the baseline in all ischemic animals. This was followed by a gradual return to 87 ± 10% and 83 ± 8% of the initial amplitude after 30 min of reperfusion in group 1 and group 2, respectively (P > 0.05). The average neurological score was significantly higher in group 1 than in group 2 at 48, 72 and 96 h after the ischemic insult (P < 0.05). Histological observations were clearly correlated with the neurological findings. Conclusion: The results suggest that subcutaneous MgSO4 reduces cerebral injury and preserves neurologic function when given two days before the transient global ischemia in rats.