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目的研究山莨菪碱对海马ＡＴＰ和ＡＴＰ酶活性的影响。方法建立沙鼠全脑缺血再灌注模型，脑缺血时间１０ｍｉｎ。动物分为假手术组，常温缺血组，常温缺血再灌注组，山莨菪组，每组８只动物。测定脑缺血后和再灌注３０及６０ｍｉｎ时海马突触体ＡＴＰ和ＡＴＰ酶活性。结果脑缺血后ＡＴＰ与缺血前后相比明显下降（Ｐ＜０．０１），常温再灌注３０ｍｉｎ时，ＡＴＰ恢复到缺血前的６４％。山莨菪碱组ＡＴＰ含量明显高于常温组（Ｐ＜０．０５）。沙鼠脑缺血１０ｍｉｎ后Ｎａ＋，Ｋ＋－ＡＴＰ酶和Ｃａ２＋－ＡＴＰ酶活性明显降低（Ｐ＜０．０５），再灌注后Ｎａ＋，Ｋ＋－ＡＴＰ酶和Ｃａ２＋－ＡＴＰ酶的活性有所恢复，但明显低于假手术组（Ｐ＜０．０５）。亚山莨菪碱组Ｎａ＋，Ｋ＋－ＡＴＰ酶和Ｃａ２＋－ＡＴＰ酶的活性明显高于常温再灌注组（Ｐ＜０．０５）。结论脑缺血后山莨菪碱治疗可促进海马突触体ＡＴＰ和ＡＴＰ酶活性的恢复，这可能是其减轻脑缺血再灌注损伤的机制之一。
Objective To study the effect of anisodamin on ATPase and ATPase activity in hippocampus. Methods The model of gerbil global cerebral ischemia / reperfusion was established. The cerebral ischemia time was 10 min. Animals were divided into sham operation group, normal temperature ischemia group, normal temperature ischemia reperfusion group, Anisodus group, each group of 8 animals. The activities of ATPase and ATPase in hippocampal synaptosomes were measured after 30min and 60min reperfusion after cerebral ischemia. Results Compared with before and after ischemia, ATP decreased significantly after cerebral ischemia (P <0.01). At 30 minutes after reperfusion, ATP returned to 64% before ischemia. The ATP content in anisodamine group was significantly higher than that in normal temperature group (P <0.05). The activities of Na +, K + -ATPase and Ca2 + -ATPase in gerbils after cerebral ischemia were significantly decreased (P <0.05), and the activities of Na +, K + -ATPase and Ca2 + -ATPase recovered after reperfusion Significantly lower than sham operation group (P <0.05). The activities of Na +, K + -ATPase and Ca2 + -ATPase in Asanisole group were significantly higher than those in normal temperature reperfusion group (P <0.05). Conclusion Anisodamine treatment after cerebral ischemia can promote the recovery of ATPase and ATPase activity in the hippocampal synapse, which may be one of the mechanisms to reduce cerebral ischemia-reperfusion injury.