Janse M J, Capucci A, Coronel R, Fabius M A
Eur Heart J. 1985 Nov;6 Suppl D:41-52. doi: 10.1093/eurheartj/6.suppl_d.41.
Normal hearts: Refractory periods were determined at 12 to 15 intramural sites of the normal canine left ventricle during steady state regularly driven rates, after each of a series of four early premature beats, and after a long pause following a series of three premature beats. The dispersion in recovery of excitability, defined as the standard deviation of the mean refractory periods, was in absolute terms the same for all three situations. However, since mean refractory periods shortened after premature beats, in relative terms, dispersion of recovery of excitability was greatest after a series of four premature beats. The refractory periods of the specialized conducting system determined during the initial beats of a new, faster rate, showed that in subsequent beats, the refractory periods of the bundle branches are alternatively shorter and longer than the refractory period of the ventricular myocardium. An example of 'concealed bundle branch re-entry' is shown. It is concluded that normal hearts are well protected from sustained arrhythmias induced by changes in rate and rhythm. Ischaemic hearts: In isolated, Langendorff perfused porcine hearts, regional ischaemia was produced by clamping the left anterior descending coronary artery. The transmembrane potentials then were recorded within a distance of less than 1 mm from a stimulating electrode in the ischaemic zone. Refractory periods in the central ischaemic zone lengthened, those in the border zone shortened. Recovery of excitability in an ischaemic myocardium cannot be expressed in terms of intervals between stimuli alone: the quality of the premature response must also be taken into account. Typically, responses elicited well after completion of repolarization have markedly reduced amplitudes and upstroke velocities. Thresholds for stimulation increase in an ischaemic myocardium, and the use of strong test stimuli leads to artefactual results: evidence is presented that strong premature stimuli excite less injured cells far away from the stimulus site. Premature stimuli often induced arrhythmias. Presence of local responses in central ischaemic cells suggest regions of unidirectional block, creating circumstances where re-entry may occur. After a long pause, alternation in action potential amplitude and duration became more pronounced: possibly, a premature impulse elicited after a long pause encounters more regions of unidirectional block so that re-entry is facilitated.(ABSTRACT TRUNCATED AT 400 WORDS)
在正常犬左心室的12至15个壁内位点测定不应期，测定时处于稳态规则驱动心率下，在一系列四个早期早搏中的每一个之后，以及在一系列三个早搏后的长时间停顿之后。兴奋性恢复的离散度，定义为平均不应期的标准差，在这三种情况下绝对值相同。然而，由于早搏后平均不应期缩短，相对而言，在一系列四个早搏后兴奋性恢复的离散度最大。在新的更快心率的初始搏动期间测定的特殊传导系统的不应期表明，在随后的搏动中，束支的不应期交替地短于和长于心室心肌的不应期。展示了一个“隐匿性束支折返”的例子。结论是正常心脏能很好地抵御由心率和节律变化诱发的持续性心律失常。缺血性心脏：在离体的、Langendorff灌注的猪心脏中，通过夹闭左前降支冠状动脉产生局部缺血。然后在缺血区距刺激电极不到1毫米的范围内记录跨膜电位。中央缺血区的不应期延长，边缘区的不应期缩短。缺血心肌中兴奋性的恢复不能仅用刺激间隔来表示：还必须考虑早搏反应的质量。通常，在复极化完成后很久引发的反应具有明显降低的幅度和上升速度。缺血心肌中的刺激阈值增加，使用强测试刺激会导致人为结果：有证据表明强早搏刺激会激发远离刺激部位的损伤较轻的细胞。早搏刺激常诱发心律失常。中央缺血细胞中存在局部反应提示存在单向阻滞区域，从而创造了可能发生折返的条件。长时间停顿后，动作电位幅度和时程的交替变得更加明显：可能，长时间停顿后引发的早搏冲动会遇到更多单向阻滞区域，从而促进折返。（摘要截取自400字）
