Kinetic effects of FPL 64176 on L-type Ca 2+ channels in cardiac myocytes
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The electrocardiogram is a graphic representation of the electrical forces produced by the heart. Muscular contraction is preceded by depolarization of the cell membranes, during which the electrical charges on the surface of the muscle fibers change from positive to negative. Depolarization is followed by repolarization, whereby the cell membrane is restored to the resting state and the charge becomes positive once again. These processes depend on the movement of ions, particularly potassium, across the cell membranes.
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Immediately after adsorption, phages T4 and T5 induce a partial depolarization of the host cytoplasmic membrane. Infected bacteria respond to this phage-induced effect by a repolarization that leads to a new steady state of reduced membrane potential. The rate and extent of repolarization are adjusted to the intensity of depolarization, which depends on the number of adsorbed phages. Consequently, the new steady state membrane potential is attained in the same interval of time regardless of the maximum depolarization. These membrane potential changes appear to be independent of phage-specific properties (type of phage, presence of DNA and internal proteins, injection process) and of several membrane-related parameters (temperature, external pH, preinfectious level of membrane potential). We propose that phage adsorption to the outer membrane triggers the emission of a signal that is transmitted to the cytoplasmic membrane. Additivity of independent signals is possible when stimuli (phages) are added at the same time. Additional adsorption of phages has no further depolarizing effect as soon as the repolarization begins. We propose that this refractoriness to secondary depolarization nd the shut-off of the first depolarization are induced by the same chemical modification also initiated by adsorption of the first phage.
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Instability of the inner mitochondrial membrane potential (ΔΨm) has been implicated in electrical dysfunction, including arrhythmogenesis during ischemia-reperfusion. Monitoring ΔΨm has led to conflicting results, where depolarization has been reported as sporadic and as a propagating wave. The present study was designed to resolve the aforementioned difference and determine the unknown relationship between ΔΨm and electrophysiology. We developed a novel imaging modality for simultaneous optical mapping of ΔΨm and transmembrane potential (Vm). Optical mapping was performed using potentiometric dyes on preparations from 4 mouse hearts, 14 rabbit hearts, and 7 human hearts. Our data showed that during ischemia, ΔΨm depolarization is sporadic and changes asynchronously with electrophysiological changes. Spatially, ΔΨm depolarization was associated with action potential duration shortening but not conduction slowing. Analysis of focal activity indicated that ΔΨm is not different within the myocardium where the focus originates compared with normal ventricular tissue. Overall, our data suggest that during ischemia, mitochondria maintain their function at the expense of sarcolemmal electrophysiology, but ΔΨm depolarization does not have a direct association to ischemia-induced arrhythmias.
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The article discusses the issues of possible connection between mechanical phenomena in myocardium and the electrical processes. Not only cardiomyocytes, but also cardiac fibroplastic are considered as substratum for the mechanisms of mechano-electrical feedbacks. Cardiomyocytes and fibroplastic of healthy animals demonstrate the mechano-electrical feedbacks, which essentially mean that stretching of the cardiac tissue within the physiological limits to 2 mN changes the electrophysiological cell processes. Close to 90% repolarization potential of cardiomyocytes action the mechano-induced depolarization develops; over the background of depolarization, when it reaches the threshold values, extra potentials of action are generated. In fibroplastic, membrane mechano-induced hyperpolarization develops; as result of cellular interaction it may develop hyperpolarization of pacemaking cells of the right auricle and slow the cardiac rythm down. In case of a pathology, for instance, infarct of the left heart ventricle modification of electric cell activity was detected at quite low values of tissue stretching up to 0.2. mN. Mechano-induced depolarization of cardiomyocytes of animals affected by infarct develops at 50% level of repolarization phase of action potential, or at 90% of repolarization phase. In the former case development of mechano-induced depolarization coincides with the period of absolute cell refractering. Extra action potential develops immediately after the refractering phase when the mechano-induced depolarization shifts the membrane potential towards threshold values. In the latter case the mechano-induced depolarization transforms into extra action potential. With further stretching fibrillation develops. In fibroplastic the values of mechano-induced membrane hyperpolarization grow with greater scope of infarct damage. Magnitude of mechano-induced hyperpolarization of auricle fibroplastic taken from the animals with infarcts shows dependence on the period of remodelling if stretching is tissue is a standard parameter. With prolongation of the remodelling period the value of mechano-induced fibroplastic hyperpolarization diminishes. The problem of developing the combinations eliminating mechano-induced cardiac arrhythmia is raised.
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