Deficiency of interfibrillar mitochondria in post-acute myocardial infarction heart failure

Abstract

Mitochondrial dysfunction plays an important role in the progress of heart failure (HF). A pronounced variability of defects in mitochondrial subpopulations is reported to occur in various disease models. The aim of the study was to define the defects in the ultra structure and bioenergetic function of cardiac mitochondria in acute myocardial infarction-induced HF. AMI-induced HF rats were treated with saline (4.0ml/kg) for 8weeks. The ultra structure of myocardial mitochondrial subpopulations was assessed by electron microscope. The bioenergetic function of myocardial mitochondrial subpopulations was evaluated through Clark oxygen electrode. Results indicated that myocardial mitochondrial subpopulations in Model group had abnormal mitochondrial morphology which manifested as swelling and vacuoles, membrane lysis, fuzzy ridge structure, cristae lysis or disappear in IFM particularly, while SSM was almost survived in AMI induced heart failure. Results showed that the oxidative phosphorylation function of respiratory chain of NADH oxidation was impaired notably. Compared with Sham group, both P/O (P<0.01) and OPR (P<0.01) of myocardial IFM in model rats decreased, and V3 (P<0.01), P/O (P<0.05) and OPR (P<0.01) of SSM in Model group decreased either. Meanwhile, the oxidative phosphorylation function of respiratory chain of FADH oxidation was injured in SSM particularly, which presented as the decreased P/O (P<0.01). We propose that the mitochondrial defect of severe HF mostly lies in the interfibrillar mitochondria rather than in the subsarcolemmal mitochondria.