Adaniya H, Hayami H, Hiraoka M, Sawanobori T
Department of Cardiovascular Diseases, Tokyo Medical and Dental University, Japan.
J Cardiovasc Pharmacol. 1994 Nov;24(5):721-9. doi: 10.1097/00005344-199424050-00006.
We examined the effects of Mg2+ on aconitine-induced polymorphic ventricular tachycardias (PVT) in excised rabbit hearts under Langendorff perfusion and in Purkinje-muscle preparations. Local electrograms using bipolar electrodes and transmembrane potentials with the microelectrode technique were recorded from Langendorff hearts and Purkinje-muscle preparations, respectively. In Langendorff preparations, intracoronary application of 0.1 microM aconitine induced PVT 28.8 +/- 3.4 min after development of regular monomorphic ventricular tachycardias (MVT) in all 18 preparations. Application of 5 and 10 mM Mg2+ restored aconitine-induced PVT to sinus rhythm after 26.8 +/- 3.4 min (n = 9), but < 3 mM Mg2+ was not effective in restoring of sinus rhythm. Increased Mg2+ concentrations < or = 5 mM in the coronary perfusate prevented development of PVT by aconitine. Intracoronary application of 10 microM tetrodotoxin (TTX) also restored aconitine-induced PVT to sinus rhythm after 3.2 +/- 0.8 min (n = 4). Although applications of 50 microM lidocaine, 10 microM flecainide, or 1 microM verapamil could change PVT to MVT, they were not effective in restoring sinus rhythm. In Purkinje-muscle preparations, spontaneous action potentials (AP) from slow diastolic depolarization appeared after aconitine at the maximum diastolic potential of -75.0 +/- 3.7 mV in Purkinje fibers and were conducted to ventricular muscles (n = 5). Spontaneous activity gradually increased in rate and then developed triggered activity arising from early after depolarization (EAD). EAD induced by aconitine always appeared first in Purkinje fibers and later in muscle fibers. Once triggered activities started from EAD, rate, rhythm and amplitudes of APs became fast and variable.(ABSTRACT TRUNCATED AT 250 WORDS)
我们研究了镁离子（Mg2+）对离体兔心脏在Langendorff灌注下以及在浦肯野肌制备物中乌头碱诱导的多形性室性心动过速（PVT）的影响。分别使用双极电极从Langendorff心脏和浦肯野肌制备物记录局部电图，并用微电极技术记录跨膜电位。在Langendorff制备物中，冠状动脉内应用0.1微摩尔/升乌头碱在所有18个制备物中，在规则的单形性室性心动过速（MVT）出现后28.8±3.4分钟诱导出PVT。应用5和10毫摩尔/升的Mg2+在26.8±3.4分钟后（n = 9）使乌头碱诱导的PVT恢复为窦性心律，但<3毫摩尔/升的Mg2+在恢复窦性心律方面无效。冠状动脉灌注液中Mg2+浓度增加至≤5毫摩尔/升可防止乌头碱诱导PVT的发生。冠状动脉内应用10微摩尔/升的河豚毒素（TTX）在3.2±0.8分钟后（n = 4）也使乌头碱诱导的PVT恢复为窦性心律。尽管应用50微摩尔/升利多卡因、10微摩尔/升氟卡尼或1微摩尔/升维拉帕米可使PVT转变为MVT，但它们在恢复窦性心律方面无效。在浦肯野肌制备物中，乌头碱作用后，浦肯野纤维在最大舒张电位-75.0±3.7毫伏时出现来自缓慢舒张期去极化的自发动作电位（AP），并传导至心室肌（n = 5）。自发活动的速率逐渐增加，然后出现由早期后去极化（EAD）引起的触发活动。乌头碱诱导的EAD总是首先出现在浦肯野纤维中，随后出现在肌纤维中。一旦触发活动从EAD开始，AP的速率、节律和幅度就会变快且多变。（摘要截断于250字）
