摘要
以尖端扭转型室速（ＴｄＰ）犬为实验模型，应用接触电极导管及针电极记录犬左心室心内膜单相动作电位（ＭＡＰ）及双极电图，探讨ＴｄＰ的发生机理及硫酸镁的治疗原理。给中毒剂量的奎尼丁后，１１只犬的ＱＴＵ间期和单相动作电位时间（ＭＡＰＤ９０）均明显延长，体表心电图上可见巨大Ｕ波，ＭＡＰ上可见早期后除极（ＥＡＤ），１１只犬均未出现自发性的ＴｄＰ。经右室程序刺激后，３只大诱发ＴｄＰ，８只犬结扎冠状动脉前降支后重复右室程序刺激，５只犬诱发出ＴｄＰ。静注硫酸镁后３阵持续性ＴｄＰ终止，Ｕ波和ＥＡＤ消失，ＱＴ间期和ＭＡＰＤ９０无明显改变。研究结果表明，ＥＡＤ可能为体表心电图异常Ｕ波的来源；奎尼丁诱发ＴｄＰ的机理：在心脏无基础病变时可能为触发活动，急性心肌缺血时可能为触发和折返；硫酸镁治疗ＴｄＰ的原理主要为抑制触发活动。
A dog model of torsades de pointes
(TdP)was developed by a toxic dose of quinidin. Left ventricular endocardial monophasic action
potential (MAP) and bipolar electrogram were recorded by endocardial contact electrode and
plunge-needle electrodes to investigate the mechanism of TdP. The effects of sulphuricum
magnesium on TdP also were examined. In 11 dogs, 30mg/kg iv quinidine prolonged QTU
interval from 240±19ms to 415±74ms (P<0.01) ,MAP duration(MAP D90) from 223±18ms to
348±82ms (P<0.01). MAP recordings from 11 dogs showed a deflection on phase 3
repolarization characteristic of early afterdepolarization(EAD) . The EAD was synchronous with
the prominent U wave in surface ECG. After performing programmed right ventricular
stimulation, 3/11 (27%) dogs developed TdP. The first ventricular ectopic beat arose to the peak
or on the descending limb of EAD and U wave. The left anterior descending coronary artery
(LAD) was occluded for 15 minutes and repeat pacing studie in the remaine dog. TdP were
induced in 5/8 (63%)dog. in 2 dogs, TdP were related to EAD. in 2 dogs, TdP were associated
with delayed fragment activity and continuous electrical activity on the bipolar electrogram
recording in accordance with a reentrant mechanism. In 1 dog, the mechanism of TdP was
unclear. 33. 3mg/kg sulphuricum magnesium terminated 3 episodes of sustained TdP with
abolishing EAD and U wave but no signifcant changes in the QTU interval and MAP D90. These
findings suggested that the prominent U wave in the surface ECG is due to EAD; EAD-induced
trigered activity play a significant role in the quinidine-induced TdP. Multiple mechanism are
involved in quinidine induced TdP in the circumstance of acute myocardial ischemia. The
mechanism of sulphuricum magnesium terminating TdP may due to suppress EAD-induced
trigered activity.
出处
《山东医科大学学报》
1994年第2期138-142,共5页
Acta Academiae Medicinae Shandong
关键词
奎尼丁
心动过速
电生理学
Quinidine
Tachycardia
Electrophysiology
