Kodama I, Goto J, Ando S, Toyama J, Yamada K
Circ Res. 1980 Jan;46(1):90-9. doi: 10.1161/01.res.46.1.90.
We studied the mechanism of post-overdrive suppression in superfused rabbit sinus node pacemaker cells. Small specimens of sinus node tissue isolated from rabbit hearts were driven at a fast rate (overdrive) for 10-120 seconds using single sucrose gap methods. During the control perfusion (35 degrees C Tyrode's solution), overdrive caused a progressive decrease in maximum diastolic potential (MDP), overshoot (OS), and maximum rate of depolarization at phase 0 [dV/dt)max]. After cessation of the overdrive, the rate of diastolic depolarization decreased, and the spontaneous activity was suppressed temporarily (post-overdrive suppression). MDP, OS, (dV/dt)max, and the spontaneous activity returned within a few seconds to the level observed before overdrive. Atropine (2 x 10(-6) g/ml) did not influence the effects of overdrive. After ouabain administration (3 x 10(-7) g/ml) or in low temperature perfusate (25 degrees C), the effects of overdrive were accentuated, and a marked suppression of spontaneous activity with a long pause of over several seconds was seen following the overdrive. These results suggest that the post-overdrive suppression of sinus node is attributable, at least in part, to ionic shifts following overdrive, and may be potentiated by metabolic dysfunction of pacemaker cells.
我们研究了在灌流的兔窦房结起搏细胞中过驱动抑制的机制。使用单蔗糖间隙法，以快速速率（过驱动）驱动从兔心脏分离的窦房结组织小标本10 - 120秒。在对照灌流期间（35℃的台氏液），过驱动导致最大舒张电位（MDP）、超射（OS）和0期最大去极化速率[dV/dt]max逐渐降低。过驱动停止后，舒张期去极化速率降低，自发活动被暂时抑制（过驱动后抑制）。MDP、OS、[dV/dt]max和自发活动在几秒钟内恢复到过驱动前观察到的水平。阿托品（2×10⁻⁶g/ml）不影响过驱动的效应。给予哇巴因（3×10⁻⁷g/ml）后或在低温灌流液（25℃）中，过驱动的效应增强，过驱动后可见自发活动明显抑制并伴有长达数秒的长间歇。这些结果表明，窦房结的过驱动后抑制至少部分归因于过驱动后的离子转移，并且可能因起搏细胞的代谢功能障碍而增强。
