大鼠梗塞心脏非梗塞区内超氧化物歧化酶、丙二醛、磷酸肌酸激酶变化及药物治疗效果
Changes of Superoxide Dismutase,Malondialdehyde,Creatine Phosphokinase in Non-infarcted Zone of an Infarcted Heart in Rats and Drug Treatment
-
摘要: 结扎左冠状动脉形成大鼠心肌梗塞,测定梗塞区(IZ)及非梗塞区(NIZ)中SOD、MDA、CPK及FFA,观察慢性梗塞心脏中的变化。NIZ中SOD下降,MDA增多及CPK减少。FFA增多不明显。这些变化与前文报道NIZ中去甲肾上腺素的耗竭及ATP一时性丧失相符。非梗塞区中生化改变,揭示‘易损基质’中一些特点,可解释梗塞心脏易于发生室颤的原因。由于梗塞心脏中形成一种代偿机制,使慢性梗塞心脏中其他心肌产生了心肌肥厚,从而引起这种变化。为降低心律失常的危险性,梗塞后心脏应接受药物治疗,以纠正这些改变。对梗塞心脏中存在易损基质,易于发生室颤的机理进行了探索。Abstract: A chronically infarcted rat heart performed by ligation of the left coronary artery was assayed for SOD activity, MDA, CPK and FFA in the infarcted(IZ)and non-infarcted zone(NIZ), simultunousely. In the NIZ, SOD was declined progressively and an over-pred