Electrophysiology of rabbit ventricular myocytes following sustained rapid ventricular pacing.
Electrophysiology of rabbit ventricular myocytes following sustained rapid ventricular pacing.
复制标题
持续快速心室起搏后兔心室肌细胞的电生理学。
DOI：
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发表时间：
1997
影响因子：
5
通讯作者：
I. Zucker
中科院分区：
文献类型：
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作者：
G. Rozanski;Zhi Xu;Ryan T. Whitney;H. Murakami;I. Zucker
本研究检测了从兔心脏分离的心室肌细胞在快速心室起搏 2-3 周后电生理特性的变化。起搏期结束时的左心室舒张末压比年龄匹配的对照组高近四倍，但心脏重量/体重比没有显着变化。与对照组相比，在低刺激频率下电流钳模式下记录的动作电位持续时间明显更长，并且来自起搏心脏的分离肌细胞的第一相减少。在电压钳实验中。 L 型 Ca2+ 电流 (ICa) 密度在肌细胞组之间没有差异，但起搏心脏的肌细胞中 10 µM 异丙肾上腺素引起的最大电流（+ 10 mV）大约减少 40%。相比之下，两组中 10 µM 毛喉素引起的最大 ICa 相似。起搏心脏的肌细胞中 4-氨基吡啶敏感的瞬时外向电流 (Ito) 比对照心脏低 65%（+ 60 mV）。然而，培养约 24 小时后，这些肌细胞中的 Ito 密度恢复到对照值。尽管 Ito 密度显着降低，但组间内向整流电流 (IK1) 没有差异。这些数据表明，快速起搏心脏的肌细胞中 Ito 显着且可逆地减少，这可能部分解释了动作电位形态的显着变化。尽管与对照组相比，这组肌细胞的基础 ICa 没有改变，但 β 激动剂对其的调节明显减弱，可能是通过受体密度降低或与腺苷酸环化酶的偶联所致。起搏心脏中肌细胞 K+ 和 Ca2+ 通道行为的这些变化可能与收缩力受损和心律失常有关，这是完整衰竭心脏的特征。
The present study examined changes in electrophysiological properties of ventricular myocytes isolated from rabbit hearts after 2-3 weeks of rapid ventricular pacing. Left ventricular end-diastolic pressure at completion of the pacing period was nearly four-fold greater than in age-matched controls, although there was no significant change in heart weight/body weight ratio. Action potentials recorded in current-clamp mode at low stimulation frequencies were significantly longer in duration and phase 1 diminished in isolated myocytes from paced hearts compared with control. In voltage-clamp experiments. L-type Ca2+ current (ICa) density was not different between groups of myocytes, but the maximum current (at + 10 mV) elicited by 10 microM isoproterenol was approximately 40% less in myocytes from paced hearts. In contrast, maximum ICa elicited by 10 microM forskolin was similar in both groups. The 4-aminopyridine-sensitive transient outward current (Ito) was 65% less (at + 60 mV) in myocytes from paced hearts than from control. However, after approximately 24 h in culture, Ito density in these myocytes returned toward control values. Despite marked reduction in Ito density, the inward rectifier current (IK1) was not different between groups. These data demonstrate that Ito is significantly and reversibly decreased in myocytes from rapidly paced hearts, which may partly account for marked changes in action potential morphology. Although basal ICa was not altered in this group of myocytes compared with control, its modulation by beta-agonists was markedly blunted, probably through a decrease in receptor density or coupling to adenylyl cyclase. These changes in myocyte K+ and Ca2+ channel behavior in paced hearts may relate to impaired contractility and arrhythmogenesis that is characteristic of the intact failing heart.