Regular Article
Regional Energy Metabolism of Failing Hearts Following Myocardial Infarction

https://doi.org/10.1006/jmcc.1993.1113Get rights and content

Abstract

To clucidate the relationship between functional alterations and disturbances in myocardial energy metabolism of rats with heart failure following coronary artery ligation, the left coronary artery of the rat was ligated and the time course of changes in cardiac function and myocardial energy state of the animal examined for 12 weeks after the ligation. Coronary artery ligation resulted approximately 40% infarction of the ventricle, an increase in the right ventricular weight, a decrease in left ventricular developed pressure, an increase in left ventricular end-diastolic pressure throughout the experiment, suggesting the development of cardiac failure after the operation. Cardiac output and stroke volume indices were not altered during the first 4 weeks, but were significantly decreased on the 8th and 12th weeks, suggesting that cardiac function had further aggravated by 8 weeks after the operation. Myocardial energy profiles of the scar tissue, the remaining left ventricle and interseptum, and the right ventricle were determined. Tissue ATP (27.54 ± 0.82 to 26.38 ± 1.58 μmol;/g dry tissue; n = 8-10) and creatine phosphate (26.73 ± 1.63 to 24.38 ± 1.83 μmol/g dry tissue; n = 8-10) of the remaining viable left ventricle were lower than control (33.17 ± 0.73 and 40.04 ± 1.07 μmol/g dry tissue; n = 8) throughout the experiment. A marked decrease in tissue ATP and CP was seen in the scar tissue throughout the experiment. Increase in tissue lactate of the remaining left ventricle and the right ventricle were detected from 1 to 2 weeks after the operation, but returned to the control levels thereafter. Mitochondrial oxygen consumption rates of isolated myocardial bundles from the 8th and 12th weeks (21.03 ± 2.22 and 17.79 ± 3.24 ng oxygen/min/mg dry tissue; n = 8) were lower than control (33.15 ± 1.95 ng oxygen/min/mg dry tissue; n = 5), and those of the interseptum (23.71 ± 1.33 ng oxygen/min/mg dry tissue; n = 8) and the right ventricle (22.44 ± 2.73 nd oxygen/min dry tissue; n = 8) on the 12th week after the operation were lower than control (33.58 ± 2.80 and 34.83 ± 2.64 ng oxygen/min/mg dry tissue; n = 5). The results provided evidence for a decline in myocardial energy store and energy producing ability associated with the development of cardiac failure.

References (0)

Cited by (101)

  • Heat-shock protein 90 modulates cardiac ventricular hypertrophy via activation of MAPK pathway

    2019, Journal of Molecular and Cellular Cardiology
    Citation Excerpt :

    The CM was separated by SDS-PAGE for western analysis of natriuretic peptide A (ANP). MI of rats was produced by ligation of the left ventricular (LV) coronary artery according to the method described previously [12]. Rats with myocardial infarction (coronary artery ligation (CAL) rats) and having an infarct area comprising approximately 40% of the left ventricle are consistently produced under our experimental conditions [13].

  • Effects of cardiosphere-derived cell transplantation on cardiac mitochondrial oxygen consumption after myocardial infarction in rats

    2018, Biomedicine and Pharmacotherapy
    Citation Excerpt :

    Heart failure represents the final common endpoint for various heart diseases, leading to cardiovascular death. In previous studies, we showed that decreased mitochondrial energy-producing ability in the remaining viable left ventricle was associated with the development of chronic heart failure following myocardial infarction in rats [1,2]. Therefore, it might be expected that preservation of mitochondrial function in the viable myocardium would play a key role in preventing the development of heart failure after a myocardial infarction.

  • Mitochondrial function in heart failure: The impact of ischemic and non-ischemic etiology

    2016, International Journal of Cardiology
    Citation Excerpt :

    In the human heart, 90% of ATP is produced by OXPHOS, therefore, an attenuation of this process in HF constitutes a major concern in terms of cardiac energy production [6,25,26]. Indeed, the current study confirms and extends previous work that has typically observed attenuated Complex I state 3 respiration in both animal models of HF and patients with HF [13,27,28]. Specifically, this study documents a HF-related attenuation in OXPHOS, per mg of tissue, assessed as Complex I, Complex II, and Complex I + II state 3 respiration, falling progressively from HdH to niHF, to iHF.

  • Protective effect of geranylgeranylacetone via enhanced induction of HSPB1 and HSPB8 in mitochondria of the failing heart following myocardial infarction in rats

    2014, European Journal of Pharmacology
    Citation Excerpt :

    In our previous study, we showed that the contents of HSPB1 and HSPB8 were decreased in the mitochondrial fraction in the failing rat heart following myocardial infarction (Marunouchi et al., 2013). In the failing heart, the energy-producing ability of cardiac mitochondria is impaired (Sanbe et al., 1993). Although, those findings suggested that decreases in HSPB1 and HSPB8 contribute to the development of heart failure, roles of these heat shock proteins in the genesis and development of mitochondrial dysfunction in the failing heart remain unclear.

View all citing articles on Scopus
View full text