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目的：观察水杨酸镁对缺血再灌注造成的脑损伤的保护作用。方法：采用四动脉结扎法，制作大鼠全脑缺血再灌注模型。动物随机分成伪手术、再灌注、尼莫地平２ｍｇ／ｋｇ、水杨酸镁５ｍｇ／ｋｇ及１０ｍｇ／ｋｇ组共５组，于缺血前，再灌注前及再灌注过程中各ｉｖ给药１次。结果：缺血４０ｍｉｎ再灌注１ｈ后，脑水份从７９．０％升到８３．２％，脑钙含量由１７３升到２３９μｇ／ｇｄｗ，丙二醛含量从１５．６升到２４．６μｍｏｌ／ｇ蛋白质，乳酸脱氢酶含量由２０．７降到１１．２ＫＵ／ｇ蛋白质。尼莫地平和水杨酸镁均能减弱上述改变，并改善再灌注期间脑电图的改变。结论：水杨酸镁保护脑组织，其机制与其钙拮抗作用有关
Objective: To observe the protective effect of magnesium salicylate on brain injury induced by ischemia-reperfusion. Methods: A rat model of global cerebral ischemia-reperfusion was established by four-artery ligation. The animals were randomly divided into sham operation, reperfusion, nimodipine 2mg / kg, magnesium salicylate 5mg / kg and 10mg / kg group of 5 groups before ischemia, before reperfusion and reperfusion each iv administration 1 Times. Results: After reperfusion for 40 minutes, the content of brain water rose from 79.0% to 83.2%, the content of brain calcium increased from 173 to 239μg / gdw, the content of malondialdehyde increased from 15.6 to 24.6μmol / g protein, lactate dehydrogenase content decreased from 20.7 to 11.2KU / g protein. Both nimodipine and magnesium salicylate attenuated these changes and improved the EEG changes during reperfusion. Conclusion: The protective mechanism of magnesium salicylate on brain tissue is related to the mechanism of calcium antagonism