The microelectrode array (MEA) was used to study excitable and non-excitable cells in the present study. Pharmacologic preconditioning effects of adenosine triphosphate-sensitive potassium (K_ATP) channel activation using potassium channel openers (KCOs) on rat cardiomyocytes and atrial slices were studied using the MEA. Rat cardiac tissues pre-treated with sarcolemmal K_ATP channel opener (sarcK_ATP), but not mitochondrial K_ATP channel opener (mitoK_ATP), retained a significantly higher viability and had significant reductions in extracellular field potential (exFP) frequency, exFP amplitudes, and exFP propagation speed changes after hypoxia. Connexin 43 expression levels were lower in KCOs pre-treated cardiomyocytes than the untreated controls, and this correlated with the propagation vel...[ Read more ]

The microelectrode array (MEA) was used to study excitable and non-excitable cells in the present study. Pharmacologic preconditioning effects of adenosine triphosphate-sensitive potassium (K_ATP) channel activation using potassium channel openers (KCOs) on rat cardiomyocytes and atrial slices were studied using the MEA. Rat cardiac tissues pre-treated with sarcolemmal K_ATP channel opener (sarcK_ATP), but not mitochondrial K_ATP channel opener (mitoK_ATP), retained a significantly higher viability and had significant reductions in extracellular field potential (exFP) frequency, exFP amplitudes, and exFP propagation speed changes after hypoxia. Connexin 43 expression levels were lower in KCOs pre-treated cardiomyocytes than the untreated controls, and this correlated with the propagation velocity results obtained from the MEA. Field potential duration of neither cardiomyocytes nor slices was affected by KCOs. In terms of physiological changes, the mitoK_ATP channel opener pre-treated hearts had a reduced change in heartbeat frequency after hypoxia. The reductions in infarct size and myocardial cell volume of the hypoxic hearts suggested that mitoK_ATP channels might also play a cardioprotective role by preserving cell volume without affecting the electrophysiology of cardiac cells. Although these KCOs had cardioprotective effects on ischaemic cells and tissues, these agents on their own disrupted the exFP propagation sequence. Stimulation of mast cells by compound 48/80 or anti-IgE produced significantly different field potential shapes and durations. Data from the present study suggest that potassium efflux and chloride influx maintain a hyperpolarised membrane potential and further facilitate mast cell degranulation. These findings are in line with the amount of histamine released from the KCOs or chloride blockers pre-treated mast cells. Disodium cromoglycate, an anti-allergic drug, was used as an example to demonstrate the feasibility of using the present MEA system for the screening of ion-channel modulators on allergic responses.