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.
- Cerebral ischemia