心肌缺血再灌注Na~ K~ ATPase活性变化及鹿茸精的保护作用

目的：研究心肌缺血再灌注损伤 Ｎａ＋  Ｋ＋ Ａ Ｔ Ｐａｓｅ 活性变化，探讨鹿茸精对心肌缺血再灌注损伤的保护作用及其机理。方法：采用大鼠离体心脏灌注模型，应用电镜酶细胞化学技术观察 Ｎａ＋  Ｋ＋ Ａ Ｔ Ｐａｓｅ 定位、分布及活性变化。结果：正常心肌 Ｎａ＋  Ｋ＋ Ａ Ｔ Ｐａｓｅ 主要位于肌膜上，缺血３０ ｍ ｉｎ，酶活性显著减弱，再灌注３０ ｍ ｉｎ 及６０ ｍ ｉｎ酶活性进一步减弱或缺失，而应用鹿茸精此酶活性减弱不明显。结论： Ｎａ＋  Ｋ＋ Ａ Ｔ Ｐａｓｅ 抑制是心肌缺血再灌注损伤的主要环节，是引起钙反常的直接原因。鹿茸精通过对此酶修饰起心肌保护作用。

Protective Effects of Pantocrine on Rat Myocardium with Ischemia Reperfusion Injury by Modifying the Activity of Na K ATPase

Objective:This paper was designed to investigate the protective effects of pantocrine on rat myocardium with ischemia reperfusion injury. Methods:We examined the location, distribution, and the changes on activity of Na K ATPase in myocardium from isolated rat hearts with ischemia reperfusion injury using electron microscopic enzyme cytochemical technique. Results:Na K ATPase was located at sarcolemma in normal myocytes. The activity of Na K ATPase attenuated significantly in 30 min of ischemia. After reperfusion for 30 and 60 minutes, the activity of enzyme became even weaker. In the group treated with pantocrine, the activity of Na K ATPase did not weaken obviously in sarcolemma for myocardium with ischemia reperfusion injury. Conclusion:Depressing the activity of Na and K ATPase was a crucial link for controlling the transition of Na and K . Pantocrine exerted strongly protective effects on myocardium with ischemia reperfusion injury by ameliorating the activity of Na K ATPase. Conclusion:Depressing the activity of Na and K ATPase was a crucial link for controlling the transition of Na and K . Pantocrine exerted strongly protective effects on myocardium with ischemia reperfusion injury by ameliorating the activity of Na K ATPase. Depressing the activity of Na and K ATPase was a crucial link for controlling the transition of Na and K . Pantocrine exerted strongly protective effects on myocardium with ischemia reperfusion injury by ameliorating the activity of Na K ATPase.