Sympathetic modulation of the relation between ventricular repolarization and cycle length.
Sympathetic modulation of the relation between ventricular repolarization and cycle length.
复制标题
心室复极与周期长度之间关系的交感调节。
作者：
A. Zaza;G. Malfatto;P. Schwartz
交感神经对心室复极的影响还没有完全阐明，尽管它们与心肌梗死相关。在24只麻醉猫上，用动作电位时程（APD）和QT间期研究了交感神经对复极的控制。分别研究了右、左胸骨切除术和随后的双侧胸骨切除术或β受体阻滞剂对稳态时APD（或QT）和周期长度（CL）之间关系的影响，以及对APD适应周期长度突然变化的动力学的影响。通过不同周期的心房起搏获得稳态APD/CL（或QT/CL）关系。评估起搏周期长度突然减少约100 msec时APD适应的动力学。稳态APD/CL（QT/CL）关系由双曲函数APD = CL/[（a. CL）+ B]。由此计算两个参数：1）1/a，即在无限循环长度（APD最大值或QT最大值）下外推的APD（QT）和2）APD（或QT）发生50%总变化时的循环长度（CL 50 = B/a）。右侧胸骨切开术降低了APD max和CL 50，随后的左侧胸骨切开术或β受体阻滞剂（普萘洛尔，0.5 mg/kg）逆转了该效应。左侧胸骨切除术延长了APD max和CL 50。在两组中，双侧胸骨切除术导致这些变量进一步增加。QT/CL关系的结果相似。APD对周期长度的适应动力学可用两个指数之和来描述。第一个时间常数（τ快，约三次心跳）是不变的任何干预;第二个（τ慢）缩短右胸骨切开术和左胸骨切开术延长。进一步去除剩余的星状神经节在两组中具有相同的效果，即tau蛋白的增加缓慢。因此，交感神经支配调制的稳态依赖周期长度和动力学的适应心室复极率的突然变化。交感神经的影响是不对称的。右侧胸骨切除术缩短了APD max和QTmax，降低了CL 50，并加速APD适应新的稳态。由于这些效应可被β受体阻滞剂或左侧胸骨切除术逆转，因此它们可能是由于反射性增强的交感神经通过左侧神经流出到心室。
Sympathetic influences on ventricular repolarization are not yet fully elucidated, despite their relevance to arrhythmogenesis. The sympathetic control of repolarization, measured from an endocardial monophasic action potential duration (APD) and from the QT interval, was investigated in 24 anesthetized cats. The effects of right and left stellectomy and of subsequent bilateral stellectomy or beta-blockade on the relation between APD (or QT) and cycle length (CL) at steady state, and on the kinetics of adaptation of APD to a sudden change in cycle length were studied separately. Steady-state APD/CL (or QT/CL) relations were obtained by atrial pacing at different cycle lengths. The kinetics of APD adaptation were evaluated for a sudden decrease of approximately 100 msec in pacing cycle length. The steady-state APD/CL (QT/CL) relation was fitted by the hyperbolic function APD = CL/[(a. CL) + b]. From this, two parameters were computed: 1) 1/a, that is, APD (QT) extrapolated at infinite cycle length (APDmax or QTmax) and 2) the cycle length at which 50% of the total change in APD (or QT) occurred (CL50 = b/a). Right stellectomy reduced APDmax and CL50, an effect reversed by subsequent left stellectomy or beta-blockade (propranolol, 0.5 mg/kg). Left stellectomy prolonged APDmax and CL50. Bilateral stellectomy, in both groups, caused a further increase in these variables. Results were similar for the QT/CL relation. The adaptation kinetics of APD to cycle length was described by the sum of two exponentials. The first time constant (tau fast, about three beats) was unchanged by any intervention; the second (tau slow) was shortened by right stellectomy and prolonged by left stellectomy. The further removal of the remaining stellate ganglion had the same effect in both groups, that is, an increase in tau slow. Thus, sympathetic innervation modulates both the steady-state dependence on cycle length and the kinetics of adaptation to sudden rate changes of ventricular repolarization. The effects of sympathetic influence are asymmetrical. Right stellectomy shortens APDmax and QTmax, reduces CL50, and accelerates APD adaptation to a new steady state. Because these effects are reversed by beta-blockade or left stellectomy, they are likely to be due to a reflexly enhanced sympathetic outflow to the ventricles through the left-sided nerves.
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