A cell model for evaluating mitochondrial damage in cardiomyocytes

Abstract

Abstract Background Various cellular models were used for assessment of mitochondrial damage in cardiomyocyte, but most of them are based on silent cells without contractility. The mitochondria in cells at working should be more sensitive to toxic or reperfusion damage due to their high level mitochondrial respiration. Therefore, contracting cells can represent inotropic agent-mediated high-energy demand states. Objective To establish a cellular model to detect mitochondrial damage in cardiomyocytes at contraction. Method Freshly isolated Sprague–Dawley rat cardiomyocytes were incubated with or without bupivacaine, in the presence or absence of isoprenaline, and electrically stimulated to induce rhythmic contractions. Results Contraction under electrical field stimulation did not induce mitochondrial swelling or ROS production in DMEM; the silent cells in the presence of bupivacaine showed mild mitochondrial swelling, but contracting cells exhibited significantly higher mitochondrial swelling and increased ROS production (P < 0.05, vs. silent cells). Isoprenaline induced a further enhancement in mitochondrial swelling and ROS production in contracting cells. Conclusions Contracting cells are more sensitive to bupivacaine toxicity and could be more accurately represent mitochondrial damage in vivo condition.