目的：探讨金属硫蛋白（ＭＴ）在培养乳鼠心肌细胞缺氧预处理中的作用机制。方法：建立培养的乳鼠心肌细胞缺氧／复氧模型，检测心肌细胞预缺氧２４ｈ后ＭＴ及丙二醛（ＭＤＡ）含量，Ｎａ＋－Ｋ＋ＡＴＰ酶、Ｃａ２＋－Ｍｇ２＋ＡＴＰ酶活性的变化以及用ＭＴ抗体阻断后的相应变化。结果：缺氧预处理组ＭＴ含量及Ｎａ＋－Ｋ＋ＡＴＰ酶、Ｃａ２＋－Ｍｇ２＋ＡＴＰ酶活性显著高于对照组及缺氧／复氧组（Ｐ＜０．０５），ＭＤＡ含量显著低于缺氧／复氧组（Ｐ＜０．０１）；使用ＭＴ抗体后，酶活性则显著降低，而ＭＤＡ含量显著高于未加抗体和对照组（Ｐ＜０．０１）。结论：缺氧预处理产生大量 ＭＴ，后者可能通过减少 ＭＤＡ及促进 Ｎａ＋－ Ｋ＋ ＡＴＰ酶、Ｃａ２＋－ Ｍｇ２＋ ＡＴＰ酶的活性升高起到保护心肌的作用。 Objective: To explore the mechanism of metallothionein (MT) in cultured neonatal rat cardiomyocytes subjected to hypoxia preconditioning. Methods: The hypoxia / reoxygenation model of cultured neonatal rat cardiomyocytes was established. The contents of MT and malondialdehyde (MDA), the activities of Na + -K + ATPase, Ca2 + -Mg2 + ATPase and the activities of MT2 The corresponding change after blocking. Results: The content of MT and the activities of Na + -K + ATPase, Ca2 + -Mg2 + ATPase in hypoxic preconditioning group were significantly higher than those in control group and hypoxia / reoxygenation group (P <0.05), MDA content was significantly lower than that in hypoxia / reoxygenation group (P <0.01). After using MT antibody, the activity of MDA decreased significantly, while the content of MDA was significantly higher than that of the control without antibody and control (P <0.01). CONCLUSION: Hypoxic preconditioning produces a large amount of MT, which may protect myocardium by decreasing MDA and promoting the activity of Na + - K + ATPase and Ca2 + - Mg2 + ATPase.