Yin Hua Zhang
Seoul National University, South Korea
Biography
Cardiac metabolism is essential in myocardial contraction. Here, we analyzed the eff ect of metabolic substrates (fatty acids, pyruvate and lactate in normal Tyrode’s solution, termed NF) on myocyte contractility in rat left ventricular myocytes. Our results showed that NF signifi cantly increased myocyte contraction and intracellular Ca2+ transients. L-type Ca2+ current or Na+- Ca2+ exchanger activity was not increased and myofi lament Ca2+ sensitivity was reduced by NF, suggesting key role of myofi lament on cardiac Ca2+ homeostasis and contraction with NF. Furthermore, NF diminished insulin-dependent tyrosine phosphorylations of insulin receptor or receptor substrate and eNOS-Ser1177. Beta-adrenergic stimulation with isoprenaline signifi cantly increased spontaneous myocyte contraction during diastole in NF. Collectively, NF impairs insulin signaling and reduces bioavailability of eNOS-derived NO, which desensitizes myofi lament Ca2+ sensitivity, increases Ca2+ level and contraction. In addition, it predisposes beta-adrenergic arrhythmogenesis in cardiac myocytes. Th e results reveal that it resembles an in vitro model of cardiac metabolic syndrome
Abstract
Abstract : Functional analysis using metabolic substrates-induced in vitro model of cardiac metabolic syndrome