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目的：观察３种穿心草酮（Ｘａｎ）对缺血再灌注模型心律失常的保护作用及其机制。方法：采用整体大鼠心肌缺血再灌注模型，于结扎前３ｍｉｎｉｖ３种Ｘａｎ１ｍｇ／ｋｇ。结果：３种Ｘａｎ可不同程度地降低缺血再灌注损伤引起的室性心律失常发性率，缩短持续时间；提高超氧化物歧化酶（ＳＯＤ）的活性，减少脂质过氧化反应代谢产物丙二醛的含量，减少心肌谷草转氨酶及乳酸脱氢酶的释放量；作用强度的顺序为：ＸａｎⅠ＞ＸａｎⅢ＞ＸａｎⅡ。结论：３种Ｘａｎ具有抗心肌缺血再灌注损伤的保护作用，作用机制可能是与其降低心肌脂质过氧化及增强ＳＯＤ的活性有关；Ｘａｎ的活性与其苯环上羟自由基及甲氧基的多少及其位置有关。
OBJECTIVE: To observe the protective effect of three kinds of xanthone (Xan) on arrhythmia induced by ischemia-reperfusion injury and its mechanism. METHODS: The whole rat model of myocardial ischemia and reperfusion was used. Three kinds of Xan 1 mg/kg were administered 3 min before ligation. Results: The three kinds of Xan can reduce the rate of ventricular arrhythmia induced by ischemia-reperfusion injury to a certain extent and shorten the duration; increase the activity of superoxide dismutase (SOD) and reduce the lipid peroxidation product C. The content of dialdehyde decreased the release of myocardial aspartate aminotransferase and lactate dehydrogenase. The order of action intensity was: Xan-I> Xan-III> Xan-II. Conclusion: The three kinds of Xan have protective effects against myocardial ischemia-reperfusion injury. The mechanism may be related to the reduction of myocardial lipid peroxidation and the enhancement of SOD activity. The activity of Xan is related to the hydroxyl radicals and methoxyl groups on the phenyl ring. How much is related to its location.