The electrophoretic mobility (EPM) of rat cardiomyocytes with or without the treatment of neuraminidase was studied by cell electrophoresis. The EPM was found to change over a range from 0 to 8.67 microm s(-1)/V cm(-1), depending on ionic strength, transmembrane potential, pH value, and/or surface charges. It is interesting that zero EPM was observed but reverse of the mobility was not. These results suggested that the negative charges carried on the cardiomyocyte surface might comprehensively consist of surface sialic acid, plasmalemma proteins, phospholipids, and transmembrane potential. The aberrant electrical double layer formed between the carried negative charges and adions had a big adsorption layer and a diffusion layer whose sizes changed circularly, making only negative charges be carried on the surface of living cardiomyocytes. The special structures on the surface of cardiomyocytes probably play a considerable role in the process of cardiac electrical activity.
Aiming at the problem encountered in the previous research: during the electrical activity of cardiomyocytes, the influent ions do not seem to be directly derived from the extracellular fluid. We chose to cut in from the colloidal properties of the cells, follow the basic principles of physical chemistry, and establish hypotheses along the derivation of the structural characteristics of cardiomyocytes. Through the surface ion adsorption experiment and patch clamp experiment of living cells, under the condition of sequentially reducing the concentration of Na+ in the extracellular fluid, we observed the exchange and diffusion of adsorbed ions on the cell surface; the changes of inflow INa, ICa-L and action potential; and correlation between results. The results showed that the hypothesis is true. The observed parameter changes were consistent with the fact that during depolarization of cardiomyocytes, the ions of influx were derived from the inference of adsorbed ions on the cell surface; at the same time, it also provided an objective and realistic explanation for the generation of electrocardiogram.
We applied a new idea that the potential effect can change the ion adsorption structure on the cell surface to explore the mechanism of digoxin poisoning and the regulation of ion channels. The effects of digoxin on the electrophoretic mobility and behaviors (non-contraction or contraction or autorhythmicity) of cardiomyocytes were observed by single-cell electrophoresis technique (imitate the opening method of in vivo channel) and the method of decomposing surface potential components on the cells. As well as affect the association with electrical activity. The results suggested that the increase of cardiomyocytes transmembrane potential and the Na+–K+ exchange on the cell surface of the action potential phase 4 caused by the poisoning dose of digoxin, leading to the oscillation of adsorbed ions on the cell surface and the incomplete channel structure, which were the mechanism of cardiac ectopic beats. The results revealed that the opening of ion channels is regulated by the surface electric double layer of the cell membrane.
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