ABSTRACT
RESUMEN El nodo sinusal constituye el marcapasos fisiológico del corazón. Diferentes estados fisiopatológicos conducen a una reducción de su función, lo que es llamado en la clínica, disfunción sinusal. Sin embargo, para la mejor comprensión de su estado de enfermedad se requiere dilucidar cómo opera en condiciones normales. Las nuevas evidencias señalan que el automatismo del nodo sinusal se produce por la interacción del reloj de membrana y el reloj de calcio, lo que le confiere un fuerte carácter que lo protege contra fallas de funcionamiento. Se presentan las evidencias actuales sobre la sincronía celular dentro del nodo sinusal, así como la forma de propagación eléctrica y el acoplamiento fuente-sumidero. Además, se describen recientes hallazgos anatómicos e histológicos.
ABSTRACT The sinus node is the physiological pacemaker of the heart. Different pathophysiological conditions lead to a reduction of its function, which is clinically called sinus dysfunction. However, for a better understanding of its disease state, it is necessary to elucidate how it works under normal conditions. New evidences indicate that the automatism of the sinus node is produced by the interaction of the membrane clock and the calcium clock, which gives it a strong character that protects it against malfunctions. Current evidences on cell synchrony within the sinus node are presented, as well as the form of electrical propagation and the source-sink coupling. In addition, recent anatomical and histological findings are described.
Subject(s)
Sinoatrial Node , Biological Clocks , Cardiac ElectrophysiologyABSTRACT
Objective To investigate the potassium currents of the cardiac pacemaking cells induced and differentiated from rat mesenchymal stem cells (MSCs) modified by HCN4 gene. Methods Identified cardiac pacemaking cells were adopted as the experiment group, and the sinoatrial node cells of original infant rat cultured in the same period were regarded as the control group. Whole cell patch was used to measure the action potential of the pacemaking cells and sinoatrial node cells. Results Action potential of automatic depolarization at dilatation was recorded in both the differentiated cardiac pacemaking cells and sinoatrial node cells. There was no significant difference on amplitudes of resting potential, amplitudes and cycle of action potential [(-50?2.8) vs (-55?5.5),(-60?2.5) vs (-65?2.5),(240?57) ms vs (250?60) ms], but the field potential was much lower in cardiac pacemaking cells than the control group[(-30?2.5) vs (-55?5.5),P