首页> 外文期刊>American Journal of Physiology >Increased vulnerability to inducible atrial fibrillation caused by partial cellular uncoupling with heptanol.
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Increased vulnerability to inducible atrial fibrillation caused by partial cellular uncoupling with heptanol.

机译:由于部分细胞与庚醇解偶联而导致的诱发性房颤的易感性增加。

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摘要

We hypothesized that partial cellular uncoupling produced by low concentrations of heptanol increases the vulnerability to inducible atrial fibrillation (AF). The epicardial surface of 12 isolated-perfused canine left atria was optically mapped before and after 1-50 microM heptanol infusion. At baseline, no sustained (>30 s) AF could be induced in any of the 12 tissues. However, after 2 microM heptanol infusion, sustained AF was induced in 9 of 12 tissues (P < 0.001). Heptanol >5 microM caused loss of 1:1 capture during rapid pacing, causing no AF to be induced. AF was initiated by conduction block across the fiber leading to reentry, which broke up after one to two rotations into two to four independent wavelets that sustained the AF. Heptanol at 2 microM had no effect on the cellular action potential duration restitution or on the maximal velocity rate over time of the upstroke. The effects of heptanol were reversible. We conclude that partial cellular uncoupling by heptanol without changing atrial active membrane properties promotes wavebreak, reentry, and AF during rapid pacing.
机译:我们假设低浓度的庚醇产生的部分细胞解偶联增加了对诱导性心房纤颤(AF)的脆弱性。在1-50 microM庚醇输注之前和之后,对12个离体灌注犬左心房的心外膜表面进行光学定位。在基线时,在12个组织中的任何一个中都不会诱导持续的(> 30 s)AF。但是,在输注2 microM庚醇后,在12个组织中的9个组织中诱发了持续性AF(P <0.001)。庚醇> 5 microM在快速起搏过程中导致1:1捕获丢失,从而不会诱发房颤。房颤是由跨纤维的传导阻滞引起的,导致折返,再折返一到两圈,分成两到四个独立的小波,从而维持房颤。浓度为2 microM的庚醇对细胞动作电位持续时间的恢复或上冲时间的最大速度没有影响。庚醇的作用是可逆的。我们得出的结论是,在不改变心房活动膜特性的情况下,通过庚醇进行的部分细胞解偶联会促进快速起搏期间的波折,折返和房颤。

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