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目的:观察急性脑梗死镁钙含量的变化,探讨其潜在机制。方法:用栓线法制成大脑中动脉阻塞梗死模型(MCAO),在MCAO后6h、12h分别测定梗死侧、对侧脑皮质匀浆及血清镁、钙含量。结果:MCAO 6h后缺血区脑皮质匀浆镁含量明显低于、钙含量明显高于健侧脑皮质区及对照组,血清镁钙含量与对照组比较无显著差异;MCAO 12h后,缺血区脑皮质匀浆镁含量进一步下降、钙含量进一步升高与对照组及MCAO 6h组比较有显著差异(P＜0.001),同时血清镁下降、钙升高(与对照组及MCAO 6h组比,P＜0.001)。结论:急性脑梗死时缺血区脑组织及血清镁含量下降、钙含量升高;镁参与了缺血性脑坏死的病理生理过程。
Objective: To observe the changes of magnesium and calcium in acute cerebral infarction and to explore its underlying mechanism. Methods: Middle cerebral artery occlusion infarction model (MCAO) was made by thread plug method. The content of magnesium and calcium in infarction side and contralateral cerebral cortex and serum were measured at 6h and 12h after MCAO. Results: The content of magnesium in ischemic cerebral cortex homogenate was significantly lower than that in control group after MCAO for 6 hours, and the content of calcium in serum was significantly higher than that in contralateral cortex and control group. After 12 hours of MCAO, Compared with control group and MCAO 6h group, magnesium content in cerebral cortex homogenate decreased further (P <0.001), serum magnesium decreased and calcium increased (compared with control group and MCAO 6h group, P <0.001). Conclusion: The content of magnesium and the content of magnesium in brain tissue and serum in acute cerebral infarction are decreased and the content of calcium is increased. Magnesium participates in the pathophysiological process of ischemic brain injury.