Vos M A, Gorgels A P, Leunissen J D, van Deursen R T, Wellens H J
Department of Cardiology, University Hospital Maastricht, The Netherlands.
Circ Res. 1991 Jan;68(1):38-44. doi: 10.1161/01.res.68.1.38.
Ouabain-induced arrhythmias are a well-known model used to study triggered activity resulting from delayed afterdepolarizations. In the intact heart, initiation of these arrhythmias is promoted by pacing, especially at fast rates. However, the relevance of the number of stimuli is unknown. In conscious dogs with formalin-induced atrioventricular block, we investigated the effect of variations in pacing mode on 1) the behavior of nonsustained triggered rhythms at progressive levels of ouabain intoxication, and 2) the induction of sustained ventricular tachycardia (VT). Twenty experiments were analyzed. Ouabain was administered as a bolus of 40 micrograms/kg followed by continuous infusion. Every 15 minutes the pacing protocol was repeated, with a maximum of 10, until completion or induction of VT. When VT could not be initiated, the experiment was repeated at least 1 week later, adding 5-10 micrograms/kg ouabain to the bolus and increasing the infusion rate correspondingly. This was repeated until VT could be induced. Four interstimulus intervals (200, 400, 600, and 800 msec) and seven numbers of stimuli (5, 10, 20, 35, 50, 100, and 150) were given in two pacing protocols. The effect of these protocols on 1) the number of induced beats per stimulation train, 2) their first postpacing interval, and 3) induction of VT were studied. Initiation of VT occurred after 75 +/- 42 minutes. The bolus of ouabain needed to induce VT was inversely related to the body weight of the animals. Progression of ouabain intoxication resulted in 1) a significant increase in the number of induced beats per stimulation train and 2) a significant shortening of the first postpacing interval. Stimulation at a faster rate and/or more stimuli resulted in 1) a significantly pronounced increase in the number of induced beats at the higher levels and 2) a significantly shorter first postpacing interval at successive levels of ouabain intoxication.(ABSTRACT TRUNCATED AT 250 WORDS)
哇巴因诱发的心律失常是一种用于研究延迟后去极化导致的触发活动的著名模型。在完整心脏中，这些心律失常的起始会因起搏而促进，尤其是在快速起搏时。然而，刺激次数的相关性尚不清楚。在福尔马林诱导的房室传导阻滞的清醒犬中，我们研究了起搏模式变化对以下两方面的影响：1）在哇巴因中毒逐渐加重时非持续性触发节律的行为；2）持续性室性心动过速（VT）的诱发。分析了20个实验。哇巴因以40微克/千克的推注剂量给药，随后持续输注。每15分钟重复一次起搏方案，最多重复10次，直至VT完成或诱发。当无法诱发VT时，至少1周后重复实验，在推注剂量中增加5 - 10微克/千克哇巴因并相应提高输注速率。重复此操作直至能诱发VT。在两种起搏方案中给出了四个刺激间期（200、400、600和800毫秒）和七个刺激次数（5、10、20、35、50、100和150）。研究了这些方案对以下方面的影响：1）每个刺激序列诱发的搏动次数；2）它们的首次起搏后间期；3）VT的诱发。VT在75±42分钟后发生。诱发VT所需的哇巴因推注剂量与动物体重呈负相关。哇巴因中毒的进展导致：1）每个刺激序列诱发的搏动次数显著增加；2）首次起搏后间期显著缩短。更快速率和/或更多刺激的起搏导致：1）在更高哇巴因中毒水平时诱发的搏动次数显著增加；2）在哇巴因中毒连续水平时首次起搏后间期显著缩短。（摘要截短至250字）
