维生素E对再灌注心肌损伤的保护作用

PROTECTION OF VITAMIN E AGAINST MYOCARDIAL INJURY FOLLOWING CORONARY REPERFUSION

SD大鼠60只,分为对照(C)、维生素E(VitE)及超氧化物歧化酶(SOD)3组。结扎左冠状动脉(LCA)5min后开放,心肌再灌注60min。结果:再灌注后C组的左室收缩峰值压持续下降,VitE及SOD组均保持10.7～12.0kPa水平约30min。C及SOD组的室颤(VF)发生率及死亡率明显高于VitE组。心肌电镜形态计量表明VitE组的心肌细胞结构基本完整,证明VitE可保护心肌细胞不受再灌注损伤。

Sixty SD rats of either sex, weighing 150-280g , were divided into control ( C ), vitamin E(Vit E)and SOD groups. An anesthetized open-chest preparation with LCA occlusion was perfromed for 5min, and followed by 60 min reperfusion . ECG , arterial pressure (AP), left ventricular pressure ( LVP ) , dP/dt and epicardial map-ping< EMP ) were recorded at intervals of 2, 5; 2, 5, 15, 30, and 60 min after occlusion and release of the LCA. Then the muscle samples were taken from LV for electron microscopic myocardial morphometry. When the LCA was released , the LVP in the rats from Vit E and SOD rose and was maintained at the level of 1.07~12 kPa about 30 min, but that in C decreased Continuously. The morbidity rate and mortality rate of VF from C were 45%; and 40%;from Vit E 15% and 0; from SOD 50% and 25%. Electron microscopic mybcardial Cell morphometry showed that the injuries of muscle fiber and mitochondria from VitE was lower than from C. The results suggest vitamin E can protect myocardial injury during reperfusion.