Characterisation of decay of frequency induced potentiation and post-extrasystolic potentiation.
Characterisation of decay of frequency induced potentiation and post-extrasystolic potentiation.
复制标题
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
中科院分区:
文献类型:
--
作者:
H. T. ter Keurs;W. Gao;H. Bosker;A. Drake;M. Noble
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.