Intravenous administration of magnesium is only neuroprotective following transient global ischemia when present with post-ischemic mild hypothermia

We hypothesized that post-ischemic hypothermia plays an important role in magnesium mediated neuroprotection following global cerebral ischemia. To test this hypothesis, we subjected rats to 8 min of global cerebral ischemia and magnesium treatment with and without post-ischemic body temperature maintenance. In Group 1, rats received an intravenously administered loading dose (LD) of 360 μmol/kg MgSO 4 immediately before ischemia followed by a 48-h intravenous infusion (IVI) at either 60, 120 or 240 μmol/kg/h. Animal body temperature was kept at 37±0.2 °C during ischemia and between 36.6 and 37.8 °C for 6 h after ischemia. In Group 2, rats received a 360 μmol/kg MgSO 4 LD followed by a 48-h IVI of either 120 or 240 μmol/kg/h MgSO 4. In this group, body temperature following ischemia was monitored but not regulated. Control animals in Groups 1 and 2 received normal saline. Seven days after ischemia, hippocampal CA1 neurons were histologically examined. All Group 1 MgSO 4-treated and control animals demonstrated less than 6% hippocampal CA1 neuronal survival. In Group 2, the rectal temperature of MgSO 4-treated and control animals spontaneously dropped as low as 35.4 °C during the 6-h post-ischemia monitoring period. In addition, Group 2 animals that received the LD followed by an IVI of 120 or 240 μmol/kg/h MgSO 4 demonstrated 34% ( p