| Objective:Myocardial infarction induces the irreversible loss of cardiomyocytes, scar formation, and may ultimately result in congestive heart failure. Previous study showed that myocardial energetic characteristics were markedly abnormal after myocardial infarction. This study is to investigate the molecular mechanism for the abnormality of energy metabolism in a rat model of myovardial infarction and provide a reference for clinical intervention.Methods:Myocardial infarction was created in SD rats by ligation of the left anterior descending coronary artery. The rats were randomly divided into 2 groups: control group, myocardial infarction group. Animals were sacrificed at 1day, 7days, 1 month after operation and the left ventricular tissues were isolated for determination of hexokinase(HK), carnitine-acylcarnitine trans-locase(CACT), fatty acyl-CoA synthetase(ACS), citrate synthase(CS), lac-tate dehydrogenase(LDH) by ELISA.Results:Compared to the control group, the abundance and activity of these enzymes were dysregulated significantly one day post-MI (P<0.05) . The abundance and activity of these enzymes had returned to normal levels one month post-MI.Conclusion:During acute phase of myocardial infarction in rats, the abundance and activity of the key enzymes in aerobic metabolism pathways were down-regulated and the key enzymes in anaerobic metabolism pathways were up-regulated. The results provide a reference for clinical intervention .
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