Meandering and unstable reentrant wave fronts induced by acetylcholine in isolated canine right atrium.
Meandering and unstable reentrant wave fronts induced by acetylcholine in isolated canine right atrium.
复制标题
乙酰胆碱在离体犬右心房中引起的蜿蜒和不稳定的折返波前。
DOI：
10.1152/ajpheart.1997.273.1.h356
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Karagueuzian,HS
中科院分区：
文献类型：
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作者：
Ikeda,T;Wu,TJ;Uchida,T;Hough,D;Fishbein,MC;Mandel,WJ;Chen,PS;Karagueuzian,HS
乙酰胆碱（ACh）增加心房对折返的脆弱性并维持其活性较长时间的机制仍不清楚。在本研究中，我们使用高分辨率的激活地图来测试的假设，ACh促进曲折的心房折返波阵面，导致分裂和新的波阵面的产生，维持活动。在11只离体犬右心房组织（3.8 x 3.2 cm）中，在ACh（15 x 10（-6）M）灌注前后通过过早点刺激（S2）诱导折返。使用509个双极电极（1.6 mm空间分辨率）构建了endocardial等时激活图，并通过动画可视化了激活波阵面的动态。发现了一个脆弱期，在此期间，S2电流强度> 4.4 +/- 2.5 mA [脆弱性下限（LLV）]和< 26 +/- 13 mA [脆弱性上限（ULV）]诱导了一个持续3 +/- 2.5 s的单一静止折返波前，周期为159 +/- 17 ms（16次发作）。AC将不应期从100 +/- 12缩短至59 +/- 9 ms（P < 0.001），并通过同时降低LLV（0.7 +/- 0.2 mA，P < 0.001）和增加ULV（82 +/- 24 mA，P < 0.01）增加对折返诱导的脆弱性。ACh加速了心率（周期为110 +/- 16 ms，P < 0.001），并将静止的折返波阵面转换为非静止（蜿蜒）的折返波阵面，显示多态性电描记图，即，“纤维化样”活动（22次发作）。再入尖端的快速弯曲导致波前破裂（18集）和新波前的产生（19集）。这些波前动力学也导致持续的（76 +/- 224 s，P < 0.001）纤颤样电描记图。我们得出结论，乙酰胆碱增加的ULV和促进曲折的一个单一的折返波前，导致解体和新的波前的产生。单一的弯曲和复杂的波前动力学引起纤颤样活动，并维持活动的持续时间较长。
The mechanism(s) by which acetylcholine (ACh) increases atrial vulnerability to reentry and maintains its activity for longer durations remains poorly defined. In the present study we used high-resolution activation maps to test the hypothesis that ACh promotes meandering of atrial reentrant wave fronts, resulting in breakup and the generation of new wave fronts that sustain the activity. Reentry was induced in 11 isolated canine right atrial tissues (3.8 x 3.2 cm) by a premature point stimulus (S2) before and after superfusion with ACh (15 x 10(-6) M). Endocardial isochronal activation maps were constructed with the use of 509 bipolar electrodes (1.6-mm spatial resolution), and the dynamics of the activation wave fronts were visualized with animation. A vulnerable period was found during which an S2 current strength > 4.4 +/- 2.5 mA [lower limit of vulnerability (LLV)] and < 26 +/- 13 mA [upper limit of vulnerability (ULV)] induced a single stationary reentrant wave front that lasted 3 +/- 2.5 s with a period of 159 +/- 17 ms (16 episodes). AC shortened the refractory period from 100 +/- 12 to 59 +/- 9 ms (P < 0.001) and increased vulnerability to reentry induction by simultaneous decrease in the LLV (0.7 +/- 0.2 mA, P < 0.001) and an increase in the ULV (82 +/- 24 mA, P < 0.01). ACh accelerated the rate (period of 110 +/- 16 ms, P < 0.001) and converted the stationary reentrant wave front to a nonstationary (meandering) reentrant wave front showing polymorphic electrograms, i.e., “fibrillation-like” activity (22 episodes). Rapid meandering of the reentry tip led to wave front breakup (18 episodes) and the generation of new wave fronts (19 episodes). These wave front dynamics also led to sustained (76 +/- 224 s, P < 0.001) fibrillation-like electrograms. We conclude that ACh increases the ULV and promotes meandering of a single reentrant wave front, leading to breakup and the generation of new wave fronts. Single meandering and complex wave front dynamics cause fibrillation-like activity and sustain the activity for longer duration.