钠泵衰竭在心肌缺血再灌注损伤中的作用

Sodium Pump Failure in Injuries after MyocardialIschemia and Reperfusion

应用Ｎａ￣＋－Ｋ￣＋ＡＴＰ酶组化方法原位表达及生化方法定量测定钠泵活性在心肌缺血再灌注损伤中的变化。结果：心肌缺血３０ｍｉｎ膜结构原位钠泵活性明显减弱，再灌注３０ｍｉｎ及６０ｍｉｎ进一步减弱或缺失；定量酶活性变化基本与原位酶活性变化一致。本研究进一步揭示心肌缺血再灌注钠泵衰竭是心肌“顿抑”等再灌注损伤表现的决定影响因素。

he changes of the activity in Na+-K-pump in situ were observed histochemically and biochemical-ly in isolated rat hearts with ischemia and reperfusion. The activity of Na+ pump in myocardiu mem-brane in situ was depressed significantly after 30 minutes of ischemia.The situation became worse in 30 and 60 minutes after reperfusion. ATPase biochemical assay indicated that the activity of Na+-K+AT-Pase was suppressed 30 minutes after ischemia and 60 minutes after reperfusion(P<0.05).Even though it recovered slightly 30 minutes after reperfusion,The slight divergence of ATPase activity be-tween cytochemical and biochemical assay in 30 minutes afte reperfusion was due to different methodolo- gy.Our study indicated that the Na pump failure played a decisive role in myocardial stunning in injuries after ischemia and reperfusion.