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。
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-preduction of MDA and chronic depletion of CPK were also noticed. An increase in FFA was not significant.These changes are compatable with the depletion of norepinephrine and a temporal loss in ATP in NIZ as reported previously. It shows some insight of 'vulnerable subetrate',responsible to the predispostion of an infarcted heart to ventricular fibrillation.Thase changes may be a consequence of hypertrophy of the rest of myocardium, which is caused. in an infarcted beart by a compensatory mechanism.It,therefore, is reasonable for a chronically infarcted heart to be treated with drugs to reduce the risk of arrhythmogenesis.
出处
《中国药科大学学报》
CSCD
北大核心
1995年第5期291-296,共6页
Journal of China Pharmaceutical University
关键词
心肌梗塞
超氧化物歧化酶
丙二醛
磷酸肌酸激酶
Myocardial infarction
Superoxide dismutase
Malondialdehyde
Creatine phosphokinase
Free fatty acid
Ventricular Hyportrophy
Propranolol
Bepridil
