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ｐｏＬ－甲状腺素４ｍｇ·ｋｇ￣（－１）·ｄ￣（－１）×７ｄ诱发大鼠心肌肥厚及左心室质膜Ｎａ￣＋，Ｋ￣＋－ＡＴＰ酶活力升高（２．３３±０２７ｖｓ１．２０±０．１４ｍｍｏｌ·ｈ￣（－１）·ｇ￣（－１）蛋白），观察维拉帕米和卡托普利对此作用的影响，经维拉帕米５和１０ｍｇ·ｋｇ￣（－１）·ｄ￣（－１）以及卡托普利５ｍｇ·ｋｇ￣（－１）·ｄ￣（－１）治疗３ｄ后，显著降低大鼠心肌肥厚程度，但不能恢复至正常状态；仅维拉帕米１０ｍｇ·ｋｇ￣（－１）·ｄ￣（－１）组鼠左心室肥厚程度显著降低。两药物均能显著降低肥厚左心室质膜Ｎａ￣＋，Ｋ￣＋－ＡＴＰ酶活力，高剂量维拉帕米可使该酶活力恢复至正常水平，提示：维拉帕米和卡托普利可能通过下调Ｎａ￣＋，Ｋ￣＋－ＡＴＰ酶活力防止心肌ＡＴＰ耗竭和缺血损伤
The myocardial hypertrophy and the Na ~ + and K ~ + -ATPase activities in left ventricular plasma of rats induced by poL-thyroxine 4mg · kg -1 (-1) · d -1 (-1) × 7d increased (2.33 ± 027vs1 .20 ± 0.14mmol · h ~ (-1) · g ~ (-1) protein), observe the effects of verapamil and captopril on this effect, the verapamil 5 and 10mg · kg ~ (-1) · d ~ (-1), and captopril 5mg · kg ~ (-1) · d ~ (-1) significantly reduced the myocardial hypertrophy in rats, but could not return to the normal state. Only verapamil 10mg · kg ~ (-1) · d ~ (-1) group left ventricular hypertrophy significantly reduced. Both drugs can significantly reduce hypertrophy of the left ventricular plasma membrane Na ~ +, K ~ + -ATP enzyme activity, high doses of verapamil can restore the enzyme activity to normal levels, suggesting: verapamil and captopril May prevent myocardial ATP depletion and ischemic injury by downregulating Na ~ +, K ~ + -ATPase activity