Respiratory Au nucleation and microelectrode techniques reveal key features of bacterial conductive matrix

Key elements of Geobacter's extracellular electron transfer mechanism are characterized combining respiratory formed gold nanoparticles with spectro-electrochemical and microelectrode techniques.

The investigation of the cellular electrophysiological and antiarrhythmic effects of a novel selective sodium–calcium exchanger inhibitor, GYKB-6635, in canine and guinea-pig hearts

The sodium–calcium exchanger (NCX) is considered as the major transmembrane transport mechanism that controls Ca2+ homeostasis. Its contribution to the cardiac repolarization has not yet been directly studied due to lack of specific inhibitors, so that an urgent need for more selective compounds. In this study, the electrophysiological effects of GYKB-6635, a novel NCX inhibitor, on the NCX, L-type calcium, and main repolarizing potassium currents as well as action potential (AP) parameters were investigated. Ion currents and AP recordings were investigated by applying the whole-cell patch clamp and standard microelectrode techniques in canine heart at 37 °C. Effects of GYKB-6635 were studied in ouabain-induced arrhythmias in isolated guinea-pig hearts. At a concentration of 1 μmol/L, GYKB significantly reduced both the inward and outward NCX currents (57% and 58%, respectively). Even at a high concentration (10 μmol/L), GYKB-6635 did not change the ICaL, the maximum rate of depolarization (dV/dtmax), the main repolarizing K+ currents, and the main AP parameters. GYKB-6635 pre-treatment significantly delayed the time to the development of ventricular fibrillation (by about 18%). It is concluded that GYKB-6635 is a potent and highly selective inhibitor of the cardiac NCX and, in addition, it is suggested to also contribute to the prevention of DAD-based arrhythmias.

Inhibitory effects of dauricine on early afterdepolarizations and L-type calcium current

We have previously reported that dauricine exerted antiarrhythmic effects on various experimental arrhythmias. To further clarify its mechanism, the effects of dauricine on action potential duration (APD), early afterdepolarizations (EADs), triangulation, which is defined as the repolarization time from APD at 30% level (APD30) to APD at 90% level (APD90), and L-type calcium current (ICa-L) were studied using standard microelectrode techniques on rabbit papillary muscles and whole-cell patch clamp techniques on single myocytes isolated from rabbits by enzymatic digestion, respectively. Cardiac hypertrophy was induced by coarctating the abdominal aorta of rabbits. The results showed that in papillary muscles of hypertrophied rabbits, 1 µmol/L dofetilide, a selective IKr blocker, prolonged APD50 and APD90 and induced EADs (4/6, p < 0.01) with hypokalemia ([K+]o = 2.7 mmol/L). Dauricine inhibited EADs (p < 0.01) and shortened the prolonged APD (p < 0.01). In single myocytes, dauricine also inhibited EADs induced by dofetilide, hypokalemia, and hypomagnesaemia. Dauricine decreased the triangulation and reduced the peak amplitude of ICa-L at all potentials tested. Dauricine shifted the steady-state activation curves to the right and steady-state inactivation curves to the left and prolonged the τ value of the recovery curve. These results suggest that dauricine inhibits EADs and this effect may be associated with its blockade of ICa-L.