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目的：研究羟苯氨酮（ｏｘｙｐｈｅｎａｍｏｎｅ，Ｏｘｙ）强心作用的生化机理。方法：采用Ｎａ＋，Ｋ＋ＡＴＰ酶活性和ｃＡＭＰＰＤＥ活性、肌浆网Ｃａ２＋ＡＴＰ酶活性和ｃＡＭＰ含量以及心肌肌原纤维Ｃａ２＋，Ｍｇ２＋ＡＴＰ酶活性等测定法，研究Ｏｘｙ对它们的影响，并与ｍｉｌｒｉｎｏｎｅ和ＭＣＩ１５４作比较。结果：Ｏｘｙ对Ｎａ＋，Ｋ＋ＡＴＰ酶和ＰＤＥ无抑制作用，也不影响心肌ｃＡＭＰ含量，但能显著增强心肌肌原纤维对Ｃａ２＋的敏感性，高浓度时轻度抑制心肌肌浆网Ｃａ２＋ＡＴＰ酶活性。结论：Ｏｘｙ的强心作用方式不同于强心苷、β受体激动剂和ＰＤＥ抑制剂等强心药，可能为一种新的钙增敏性强心药物。
Objective: To study the biochemical mechanism of cardiac function of oxyphenamone (Oxy). Methods: The effects of Oxy on them were studied by using the assay of Na +, K + -ATPase activity and cAMP-PDE activity, Ca2 + -ATPase activity and cAMP content in sarcoplasmic reticulum, Ca2 + and Mg2 + -ATPase activity in myocardial myofibrils, And with milrinone and MCI 154 for comparison. Results: Oxy had no inhibitory effect on Na +, K + -ATPase and PDE, but also did not affect the content of cAMP in myocardium, but significantly increased the sensitivity of myocardial myofibrils to Ca2 +. At high concentration, Oxygen inhibited the sarcoplasmic reticulum Ca2 + -ATP Enzyme activity. CONCLUSION: Cardiac function of Oxy is different from cardiac glycosides such as cardiac glycosides, β-agonists and PDE inhibitors, and may be a new calcium-sensitive cardiotropic drug.