Characterisation of decay of frequency induced potentiation and post-extrasystolic potentiation.

Characterisation of decay of frequency induced potentiation and post-extrasystolic potentiation.
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频率诱导增强和期外收缩后增强的衰减特征。

DOI:
10.1093/cvr/24.11.903
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发表时间:
1990
影响因子:
10.8
通讯作者:
M. Noble
M. Noble
中科院分区:
医学1区
文献类型:
--
作者:
H. T. ter Keurs;W. Gao;H. Bosker;A. Drake;M. Noble

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研究目标 其目的是通过心搏频率的衰减和早搏后的增强来阐明心搏的潜在过程。 设计 心室起搏包括一个“预充期”,然后是以1个S间隔的“衰减期”起搏,其特征是左心室(LV)dp/dtmax的递减增强;这些被识别为试搏1、2、3、4、5。增加预激频率(频率增强)和以给定的平均频率交替缩短预激间隔(成对脉冲刺激)(早搏后增强)可增加试搏1(P1)的增强幅度。测定了指数衰减常数(P2)和渐近值(P3),并与实测值和前一拍与一拍的收缩程度之间的线性关系的斜率进行了比较。衰变后的最低值与前置增强的大小有关。 实验材料 麻醉犬6只,诱导心脏传导阻滞和β-肾上腺素能受体阻滞剂。每搏间期由可编程刺激器进行的心室起搏控制。 测量方法和主要结果 每一次搏动的收缩能力由脑室内测压计获得的最大左心室压力上升速率(LVdP/dtmax)来评估。对增强衰减的指数拟合的渐近值(P3)被发现低于测量的最低值,随后LVdP/dtmax增加到最终的稳态值P4。发现衰减常数(P2)等于一个节拍的收缩幅度与前一个节拍的收缩强度之间线性关系的斜率的自然对数,在给定的平均启动频率下,它不受启动频率或间隔的影响。渐近线P3与P_1呈负相关。 结论 P1被解释为激活剂在内部释放库中积聚的表达,P3被解释为激活剂自身对激活剂进入的负反馈控制的表现,而P4的缓慢恢复是由于动作电位时程的缓慢延长和/或从细胞内代谢物或离子的积累中恢复。
STUDY OBJECTIVE The aim was to elucidate the processes underlying the beat by beat decay of frequency induced and post-extrasystolic potentiation. DESIGN 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. EXPERIMENTAL MATERIAL 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. MEASUREMENTS AND MAIN RESULTS 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. CONCLUSIONS 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.