Li H G, Jones D L, Yee R, Klein G J
Department of Physiology, University of Western Ontario, London, Canada.
Am J Physiol. 1991 Jun;260(6 Pt 2):H1973-9. doi: 10.1152/ajpheart.1991.260.6.H1973.
Defibrillation is known to cause inability to pace the heart acutely, but the mechanism is unknown. This study used microelectrode techniques to directly evaluate the effect of defibrillation shocks on the pacing threshold and membrane potentials from superfused guinea pig papillary muscles. Failure of pacing stimuli to induce action potentials (pacing failure) followed shocks of 50-200 V/cm, with pacing failure duration correlated with shock intensity. Increasing pacing strength from one to three times diastolic threshold decreased the incidence and duration of pacing failure. Decreased extracellular calcium concentration and verapamil added to the superfusate increased the duration of pacing failure. Membrane potential depolarization occurred after shock, but pacing failure did not correlate with depolarization magnitude. We conclude that defibrillation shocks directly cause shock intensity-dependent increase of myocardial pacing threshold. The pacing threshold of the myocardium can be increased after defibrillation shock independent of hypoxia or shock-induced depolarization and may involve membrane changes in calcium handling.
除颤会导致急性心脏无法起搏，这是已知的，但机制尚不清楚。本研究使用微电极技术直接评估除颤电击对豚鼠乳头肌的起搏阈值和膜电位的影响。50-200V/cm的电击后，起搏刺激无法诱发动作电位（起搏失败），起搏失败持续时间与电击强度相关。将起搏强度从舒张阈值的1倍增加到3倍可降低起搏失败的发生率和持续时间。降低细胞外钙浓度并向灌流液中添加维拉帕米会增加起搏失败的持续时间。电击后膜电位发生去极化，但起搏失败与去极化幅度无关。我们得出结论，除颤电击直接导致心肌起搏阈值随电击强度增加。除颤电击后心肌起搏阈值可升高，与缺氧或电击诱发的去极化无关，可能涉及钙处理的膜变化。
