Zhou X, Guse P, Wolf P D, Rollins D L, Smith W M, Ideker R E
Department of Medicine, Duke University Medical Center, Durham, NC 27710.
Circ Res. 1992 Apr;70(4):773-86. doi: 10.1161/01.res.70.4.773.
Although sodium channels have been reported to be inactive after 5-10 minutes of ventricular fibrillation (VF), their state during early VF is unknown. In 12 open-chest dogs, a floating glass microelectrode was used to record intracellular action potentials from the right ventricle during pacing and during electrically induced VF. Before any drug was administered, an initial episode of VF was continuously recorded for at least 20 seconds followed by defibrillation. Recordings were made during VF episodes after superfusion for 15 minutes around the microelectrode site by low (2.8 x 10(-5) M) and high (10(-4) M) concentrations of tetrodotoxin (TTX) in five dogs, or by low (4 microM) and high (100 microM) concentrations of verapamil in another four dogs. In three dogs, VF was induced without drugs three times to determine if the effects observed in the previous dogs were caused by the drugs or by successive episodes of VF. Ten consecutive action potentials were analyzed at the onset and after 5, 10, 15, and 20 seconds of VF. Action potential amplitude and duration during paced rhythm or VF were not changed by the local perfusion of either TTX or verapamil. In the TTX group, the maximum upstroke rate of depolarization of an action potential (Vmax) during paced rhythm was 104 +/- 14 V/sec for control cycles before any drug was given, 86 +/- 15 V/sec for the low TTX concentration, and 55 +/- 14 V/sec for the high TTX concentration (p less than 0.05 versus other two). Vmax decreased from 55 +/- 32 V/sec at the beginning of VF to 37 +/- 27 V/sec after 20 seconds of VF for predrug VF, from 39 +/- 20 V/sec to 18 +/- 11 V/sec for low-dose TTX VF, and from 18 +/- 13 V/sec to 12 +/- 7 V/sec for high-dose TTX VF (p less than 0.05 among the three groups). In the dogs receiving verapamil, VF was still inducible with Vmax not significantly different from predrug VF at the onset and after 5 or 20 seconds of VF but with Vmax smaller (p less than 0.05) for verapamil than for predrug VF after 10 or 15 seconds of VF. In three dogs, Vmax was not significantly different during three successive episodes of VF when no drug was given between the episodes.(ABSTRACT TRUNCATED AT 400 WORDS)
尽管有报道称钠通道在心室颤动（VF）5 - 10分钟后失活，但其在VF早期的状态尚不清楚。在12只开胸犬中，使用漂浮玻璃微电极在起搏期间和电诱导VF期间记录右心室的细胞内动作电位。在给予任何药物之前，连续记录至少20秒的初始VF发作，随后进行除颤。在5只犬中，通过在微电极部位周围以低（2.8×10⁻⁵ M）和高（10⁻⁴ M）浓度的河豚毒素（TTX）灌注15分钟后记录VF发作；在另外4只犬中，通过低（4 microM）和高（100 microM）浓度的维拉帕米灌注。在3只犬中，三次无药物诱导VF以确定在前述犬中观察到的效应是由药物还是连续的VF发作引起的。在VF开始时以及VF 5、10、15和20秒后分析连续10个动作电位。无论是TTX还是维拉帕米的局部灌注均未改变起搏节律或VF期间的动作电位幅度和持续时间。在TTX组中，在给予任何药物之前的对照周期中，起搏节律期间动作电位的最大去极化上升速率（Vmax）为104±14 V/秒，低TTX浓度时为86±15 V/秒，高TTX浓度时为55±14 V/秒（与其他两组相比，p＜0.05）。对于给药前的VF，VF开始时Vmax从55±32 V/秒降至VF 20秒后的37±27 V/秒；对于低剂量TTX的VF，从39±20 V/秒降至18±11 V/秒；对于高剂量TTX的VF，从18±13 V/秒降至12±7 V/秒（三组之间p＜0.05）。在接受维拉帕米的犬中，VF仍可诱导，VF开始时以及VF 5或20秒后的Vmax与给药前的VF无显著差异，但在VF 10或15秒后，维拉帕米组的Vmax比给药前的VF小（p＜0.05）。在3只犬中，在连续三次VF发作期间，发作之间未给予药物时Vmax无显著差异。（摘要截断于400字）
