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心肌细胞兴奋性是维持正常的心脏活动的一个重要生理因素。本研究旨在使用全细胞膜片技术探讨豚鼠心房和心室肌细胞不同兴奋性的离子机理。结果显示,心室肌细胞兴奋性比心房肌细胞低。虽然豚鼠心室肌细胞的电压门控快Na+电流(INa)密度较低,但与其兴奋性较低并不相关,因为其在阀电位附近的可用度比率比心房肌细胞高。经典内向整流钾电流(IK1)在心室肌细胞比在心房肌细胞更大,这可能是心室肌细胞兴奋性较低的部分原因。此外,去极化引起的有内向整流特性的瞬时外向钾电流(Itoir)在心室肌细胞较大,并可能是其兴奋性较低的主要原因。在心室肌细胞,5μmol/L Ba2+显著抑制Itoir,增强细胞兴奋性,并使INa激活的阈电位更负,其作用独立于对INa的影响。本研究结果证明,除经典的IK1外,Itoir在豚鼠心房肌和心室肌细胞的兴奋性差异形成和心肌兴奋性维持中起着主要作用。然而,Itoir增加是否会通过降低兴奋性以保护心脏,还需要进一步研究。
Cardiomyocyte excitability is an important physiological factor in maintaining normal cardiac activity. The aim of this study was to investigate the ionic mechanism of different excitability of atrial and ventricular myocytes in guinea pigs using whole cell patch technology. The results show that ventricular myocytes excitability lower than that of atrial myocytes. Although guinea pig ventricular myocytes have a lower voltage-gated fast Na + current (INa) density, they are not associated with their lower excitability because of their higher availability ratio near the valve potential than atrial myocytes. Classical inward rectifier potassium current (IK1) is greater in ventricular cells than in atrial myocytes, which may be partly responsible for the lower excitability of ventricular myocytes. In addition, the depolarization induced transient outward potassium current (Itoir) with inward rectifying properties is larger in ventricular myocytes and may be the main reason for its lower excitability. In ventricular myocytes, 5μmol / L Ba2 + significantly inhibited Itoir, enhanced cell excitability and more negative threshold potential for INa activation, independent of its effect on INa. Our results demonstrate that Itoir plays a major role in the formation of excitability and the maintenance of cardiac excitability in the atrial and ventricular myocytes of guinea pigs, in addition to the classical IK1. However, whether Itoir increase protects the heart by reducing excitability requires further study.