Interplay between adrenaline and interbeat interval on ventricular repolarisation in intact heart in vivo.
Interplay between adrenaline and interbeat interval on ventricular repolarisation in intact heart in vivo.
复制标题
体内完整心脏中肾上腺素和搏动间隔对心室复极的相互作用。
DOI：
10.1093/cvr/24.11.884
复制
发表时间：
1990
影响因子：
10.8
通讯作者：
Frank Harrison
中科院分区：
文献类型：
--
作者：
Peter Taggart;P. Sutton;Max J. Lab;John Dean;Frank Harrison
研究目的
目的是检验肾上腺素和心率变化之间的相互作用可能改变心室复极的正常时间顺序的假设（因此不应）的方式，（1）可能有利于心律失常的形成，（2）可能部分解释肾上腺素作用的相互矛盾的报告，即，对动作电位时程有两种相反的作用，和（3）与正常人中有时发生的T波异常有关。
设计
作为复极化时程的测量，同时记录猪心三个心外膜部位（左心室心尖部、左心室基部和右心室中部）的单相动作电位。在稳态起搏期间，以逐渐缩短的间期插入测试脉冲间期，以构建恢复曲线。
测量值和主要结果
肾上腺素输注（0.4-1.5 μ g·kg-1·min-1）导致较短心搏间期后心搏复极提前，较长心搏间期后复极延迟，倾向于使恢复曲线逆时针（即，对动作电位时程有两种相反的影响）。各区域之间的效果并不相同。为了显示这种不均匀性，使用差分输入放大器减去来自不同区域的双相动作电位对，以在放大器输出处产生ECG样波形。由此产生的T波是对其推导出的单相动作电位之间复极化时间差的测量。由肾上腺素和速率变化引起的复极的不均匀性反映在该衍生T波的形态中，特别是在早期（过早）搏动时。这些T波变化与相同记录部位之间记录的双极电描记图中的真实T波变化密切相关（R = 0.89; p <0.0001）。
结论
这些结果表明，肾上腺素改变了正常的心跳间隔和复极时间之间的关系。效果是不均匀的，当观察到区域差异时，它们反映在T波形态的变化中。这些标记间隔很短。除了肾上腺素引起的兴奋性增加外，交感神经活动增加和早期搏动的结合可能通过夸大复极化的离散度而易患心律失常。
STUDY OBJECTIVE
The aim was to examine the hypothesis that an interaction between adrenaline and change in heart rate may alter the normal time sequence of ventricular repolarisation (and hence refractoriness) in a manner that (1) may favour arrhythmia formation, (2) may partly explain conflicting reports of the effect of adrenaline, ie, there are two opposing effects on action potential duration, and (3) be relevant to T wave abnormalities that sometimes occur in normal people.
DESIGN
As a measure of the time course of repolarisation, monophasic action potentials were recorded simultaneously from three epicardial sites in the porcine heart (left ventricular apex, left ventricular base, and mid right ventricle). During steady state pacing, test pulse intervals were interposed at progressively shorter intervals in order to construct restitution curves.
MEASUREMENTS AND MAIN RESULTS
Adrenaline infusion (0.4-1.5 micrograms.kg-1.min-1) resulted in earlier repolarisation in the beats after shorter interbeat intervals, and delayed repolarisation after longer interbeat intervals, tending to turn the restitution curve anticlockwise (ie, there were two opposing effects on action potential duration). The effects were not homogeneous between regions. To show this inhomogeneity, pairs of monophasic action potentials from different regions were subtracted using a differential input amplifier to produce an ECG like waveform at the amplifier output. The resulting T wave was thereby a measure of the time difference in repolarisation between the monophasic action potentials from which it was derived. The inhomogeneity of repolarisation induced by adrenaline and rate change was reflected in the morphology of this derived T wave, particularly at early (premature) beats. These T wave changes correlated closely with the true T wave changes in bipolar electrograms recorded between the same recording sites (R = 0.89; p less than 0.0001).
CONCLUSIONS
These results show that adrenaline altered the normal relationship between interbeat interval and the timing of repolarisation. The effect was not homogeneous and when regional differences were observed they were reflected in changes in T wave morphology. These were marked at short intervals. It is possible that in addition to increased excitability observed with adrenaline, a combination of raised sympathetic activity and early beats predisposes to arrhythmias by exaggerating dispersion of repolarisation.