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Spontaneous contractions in rat cardiac trabeculae. Trigger mechanism and propagation velocity

机译:大鼠心脏小梁自发性收缩。触发机制和传播速度

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摘要

It has previously been observed that spontaneous contractions start in a region of damage of isolated right ventricular trabeculae of rat, propagate along the muscle, and induce triggered arrhythmias (Mulder, B.J.M., P.P. de Tombe, and H.E.D.J. ter Keurs. 1989. J. Gen. Physiol. 93:943-961). The present study was designed to analyze the mechanisms that lead to triggered propagated contractions (TPCs). TPCs were elicited in 29 trabeculae by stimulation with trains (2 Hz; 15-s intervals) at varied number of stimuli (n), lowered temperature (19-21 degrees C), and varied [Ca++]o (1.5-4 mM) in the superfusate. Length (SL) and shortening of sarcomeres in the muscle were measured at two sites using laser diffraction techniques; twitch force (Ft) was measured with a silicon strain gauge. Time between the last stimulus in the train and the onset of sarcomere shortening due to a TPC at a site close to the damaged end region (latency) and propagation velocity of the contraction (Vprop) were correlated with Ft. For 10 trabeculae, TPCs were calculated to start in the end region itself 586 +/- 28 ms (mean +/- 1 SEM) after the last stimulus of a train (n = 15; [Ca++]o: 1.5 mM), i.e., at the end of or after the rapid release of the damaged end during twitch relaxation. When Ft was increased by increasing either SL prior to stimulation or the afterload during twitches, methods that do not affect intracellular calcium levels, latency decreased, but Vprop remained constant. No TPC occurred when Ft was less than 20% of maximal Ft. Both increasing [Ca++]o and n increased Ft to a maximum, increased Vprop progressively (maximum Vprop, 17 mm/s), but decreased latency. These observations suggest that initiation of TPCs depends on the force developed by the preceding twitch, and therefore on the degree of stretch and subsequent rapid release of damaged areas in the myocardium, while Vprop along the trabeculae is determined by intracellular calcium concentration.
机译:先前已经观察到,自发性收缩始于大鼠离体的右心小梁的损伤区域,沿肌肉传播,并诱发触发性心律不齐(Mulder,BJM,PP de Tombe和HEDJ ter Keurs。1989. J. Gen生理学》 93:943-961)。本研究旨在分析导致触发性传播收缩(TPC)的机制。通过在不同数量的刺激(n),降低的温度(19-21摄氏度)和变化的[Ca ++] o(1.5-4 mM)下用火车(2 Hz; 15-s间隔)刺激,在29个小梁中诱发TPC。在超融合。使用激光衍射技术在两个部位测量肌肉中肉瘤的长度(SL)和缩短。用硅应变仪测量拉力(Ft)。列车中的最后刺激与因TPC在接近受损末端区域的位置(等待时间)导致的小肌节缩短开始之间的时间(收缩)和收缩的传播速度(Vprop)与Ft相关。对于10个小梁,计算出的TPC在火车的最后刺激(n = 15; [Ca ++] o:1.5 mM)之后的末端区域本身开始586 +/- 28 ms(平均+/- 1 SEM)。 ,在抽搐松弛过程中迅速释放受损末端的末端或之后。当通过增加刺激前的SL或抽搐后的后负荷增加Ft时,不影响细胞内钙水平的方法,潜伏期减少,但Vprop保持恒定。当Ft小于最大Ft的20%时,没有TPC发生。 [Ca ++] o和n的增加都将Ft增加到最大,逐渐增加了Vprop(最大Vprop,17 mm / s),但延迟降低了。这些观察结果表明,TPC的启动取决于前一次抽搐所产生的力,因此取决于伸展程度以及随后心肌中受损区域的快速释放,而沿小梁的Vprop是由细胞内钙浓度决定的。

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