Effects of elevated plasma magnesium versus calcium on cerebral ischemic injury in rats

Both Mg²⁺ and Ca²⁺ have been implicated as having roles in the pathomechanisms of cerebral ischemia. To further study the effects of these ions on postischemic histologic outcome, fasted rats were given one of three intravenous infusions: 5.0 mmol/kg MgCl₂, 5.0 mmol/kg MgCl₂+0.035 units/kg regular insulin, or 1.0 mmol/kg CaCl₂. This resulted in elevated plasma Mg²⁺ or Ca²⁺ concentrations In the corresponding groups. A fourth group received 0.9% NaCI (saline). Preinfusion plasma glucose concentration was similar for all groups and was unchanged after infusion in rats receiving either saline or MgClι+insulin. In contrast, postinfusion glucose concentration was increased in the MgCl₂ group (p<0.001) and decreased in the CaCl₂] group (p<0.001) relative to saline-treated rats. Following respective infusions, all rats underwent 10 minutes of reversible forebrain ischemia (bilateral carotid artery occlusion and systemic hypotension) followed by 7 days’ recovery. Six of 12 CaCl₂-treated rats died 2-3 days after ischemia; all other rats remained neurologically indistinguishable, without gross neurologic deficits. Histologic injury in the neocortex and caudate was moderate in all groups. In the hippocampus, MgCl₂+insulin resulted In 66±6% (mean±SD) dead CA1 pyramidal cells, which was similar to the amount in saline-treated rats (68± 10%). Injury was increased in the MgCl₂ group (79±4% dead cells), while in surviving CaCl₂-treated rats, injury was decreased (54±13%). We conclude that the increased injury in MgCl₂-treated rats and the decreased injury noted in surviving rats receiving CaCl₂are due to the plasma glucose concentrations present prior to ischemia. When glucose concentration was controlled, no cerebral protective effect of MgCl₂was evident.