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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。
The left coronary artery was ligated to form myocardial infarction in rats, and the changes of SOD, MDA, CPK and FFA in infarction zone (IZ) and non-infarction zone (NIZ) were measured. NIZ SOD decreased, MDA increased and CPK decreased. FFA increase is not obvious. These changes are in line with previously reported depletion of norepinephrine in NIZ and a temporary loss of ATP. Biochemical changes in the non-infarct zone reveal some of the features of the ’delicate matrix’ that explain why the infarct heart is prone to ventricular fibrillation. This change is caused by the formation of a compensatory mechanism in the infarct heart that produces cardiac hypertrophy in other myocardium in the chronic infarct heart. To reduce the risk of arrhythmia, the infarcted heart should be medically treated to correct these changes. The existence of a vulnerable matrix in the infarcted heart, the mechanism of which is prone to ventricular fibrillation, is explored.