Wiggins J R, Leary J M, Cranefield P F
Eur J Cardiol. 1975 Oct;3(3):181-5.
Postextrasystolic potentiation induced by paired-pulse stimulation was studied in mammalian ventricle muscle in the presence of verapamil (0.2-4.0 muM). Verapamil exerts a negative inotropic effect on the potentiated contraction, but the force of the potentiated contraction in the presence of verapamil is greater than that of the normal, unpotentiated contraction in the absence of verapamil. The positive inotropic effect of paired stimulation appears to result both from an additional calcium influx appearing as a calcium current during the plateau of the premature action potential and from some additional mechanism, tentatively identified as a Na: Ca exchange. Our results suggest that paired-pulse stimulation could be used clinically to counteract the negative inotropic effects of verapamil; moreover, the antiarrhythmic action of verapamil might counteract any arrhythmias caused by paired pacing.
在维拉帕米(0.2 - 4.0 μM)存在的情况下,对哺乳动物心室肌中由成对脉冲刺激诱导的早搏后增强进行了研究。维拉帕米对增强的收缩产生负性肌力作用,但在维拉帕米存在时增强收缩的力量大于在无维拉帕米时正常的、未增强收缩的力量。成对刺激的正性肌力作用似乎既源于在早搏动作电位平台期作为钙电流出现的额外钙内流,也源于某种额外机制,暂定为钠钙交换。我们的结果表明,成对脉冲刺激可在临床上用于抵消维拉帕米的负性肌力作用;此外,维拉帕米的抗心律失常作用可能会抵消由成对起搏引起的任何心律失常。