ter Keurs H E, Gao W D, Bosker H, Drake-Holland A J, Noble M I
Academic Unit of Cardiovascular Medicine, Charing Cross and Westminster Medical School, London.
Cardiovasc Res. 1990 Nov;24(11):903-10. doi: 10.1093/cvr/24.11.903.
The aim was to elucidate the processes underlying the beat by beat decay of frequency induced and post-extrasystolic potentiation.
The ventricular pacing protocol consisted of a "priming period" followed by a "decay" period of pacing at 1 s intervals, characterised by a decaying potentiation of left ventricular (LV) dP/dtmax; these were identified as test beats 1,2,3,4,5. The magnitude of potentiation of test beat 1 (P1) was increased both by increased priming frequency (frequency potentiation) and by alternately shorter priming intervals (paired pulse stimulation) at a given average frequency (post-extrasystolic potentiation). The exponential decay constant (P2) and the asymptotic value (P3) were determined and compared with the measured values and with the slope of the linear relationship between the contractility of one beat and that of the preceding beat. The lowest values after decay were related to the magnitude of preceding potentiation.
Six anaesthetised dogs with induced heart block and beta adrenergic blockade were used. Beat to beat interval was controlled by ventricular pacing from a programmable stimulator.
Contractility of each beat was assessed from maximum rate of rise of LV pressure (LVdP/dtmax) obtained from an intraventricular micromanometer. The asymptotic value of the exponential fit to the decay of potentiation (P3) was found to be below the measured nadir value, which was followed by an increase in LVdP/dtmax to the final steady state value P4. The decay constant (P2) was found to be equivalent to the natural logarithm of the slope of the linear relationship between the contractility of one beat and that of the preceding beat; it was unaffected by priming frequency or interval at a given average priming frequency. The asymptote P3 was inversely related to P1.
P1 was interpreted as the expression of accumulation of activator in an internal release store; P3 was interpreted as a manifestation of negative feedback control of activator entry by the released activator itself, and the slow recovery to P4 as due to the slow lengthening of action potential duration and/or recovery from accumulation of an intracellular metabolite or ion.
旨在阐明频率诱导和早搏后增强逐搏衰减的潜在机制。
心室起搏方案包括一个“预激期”，随后是以1秒间隔进行起搏的“衰减期”，其特征为左心室（LV）dP/dtmax的增强逐渐衰减；这些被确定为测试搏动1、2、3、4、5。测试搏动1（P1）的增强幅度通过增加预激频率（频率增强）以及在给定平均频率下交替缩短预激间隔（配对脉冲刺激）而增加（早搏后增强）。确定指数衰减常数（P2）和渐近值（P3），并与测量值以及一个搏动的收缩性与前一个搏动的收缩性之间线性关系的斜率进行比较。衰减后的最低值与先前增强的幅度相关。
使用了6只诱导了心脏传导阻滞并进行了β肾上腺素能阻滞的麻醉犬。逐搏间期由可编程刺激器的心室起搏控制。
通过从心室内微测压计获得的左心室压力最大上升速率（LVdP/dtmax）评估每个搏动的收缩性。发现增强衰减的指数拟合的渐近值（P3）低于测量的最低点值，随后LVdP/dtmax增加到最终稳态值P4。发现衰减常数（P2）等同于一个搏动的收缩性与前一个搏动的收缩性之间线性关系斜率的自然对数；在给定平均预激频率下，它不受预激频率或间隔的影响。渐近线P3与P1呈负相关。
P1被解释为激活剂在内部释放储存库中积累的表达；P3被解释为释放的激活剂自身对激活剂进入的负反馈控制的表现，而缓慢恢复到P4是由于动作电位持续时间的缓慢延长和/或细胞内代谢物或离子积累后的恢复缓慢。
