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首页> 外文期刊>Japanese Journal of Pharmacology >Electrophysiologic Interaction between Class I Antiarrhythmic Drugs and Volatile Anesthetics in Depressant Effects on Ventricular Activation in a Canine Myocardial Infarction Model
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Electrophysiologic Interaction between Class I Antiarrhythmic Drugs and Volatile Anesthetics in Depressant Effects on Ventricular Activation in a Canine Myocardial Infarction Model

机译:犬心肌梗死模型中I类抗心律不齐药物与挥发性麻醉药对心室激活的抑制作用之间的电生理相互作用

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References(28) Cited-By(5) Previous studies showed that volatile anesthetics depressed ventricular delayed activation in a canine myocardial infarction model. It is well known that class I antiarryhthmic drugs depress the ventricular activation in the infarcted myocardium. In the present study, we examined the electrophysiologic interaction between volatile anesthetics (sevoflurane, isoflurane) and class I antiarrhythmic drugs (lidocaine, procainamide) in effects on the ventricular delayed activation in a canine myocardial infarction model. The conduction time of the premature stimulation-induced ventricular excitation was measured in both normal and infarcted zones of the ventricle. An interval from the premature stimulus artifact to the epicardial activation was measured on bipolar electrograms as an index of conduction time, i.e., activation time. In the infarcted zone, the volatile anesthetics and class I antiarrhythmic drugs prolonged the activation time in the infarcted zone, and the combination of the volatile anesthetics and the class I antiarrhythmic drugs markedly prolonged the activation time or blocked the delayed activation. In the normal zone, a similar synergistic interaction was observed, but the effect of these drugs was less compared with that in the infarcted zone. From these results, possible mechanisms to explain the synergistic interaction were discussed.
机译:参考文献(28)Cited-By(5)先前的研究表明,挥发性麻醉药可降低犬心肌梗塞模型的心室延迟激活。众所周知,I类抗心律失常药物可抑制梗死心肌的心室激活。在本研究中,我们检查了挥发性麻醉药(七氟醚,异氟烷)和I类抗心律不齐药物(利多卡因,普鲁卡因胺)在犬心肌梗死模型中对心室延迟激活的影响。在脑室的正常区域和梗塞区域均测量了过早刺激诱发的心室兴奋的传导时间。在双极电描记图上测量从过早刺激伪像到心外膜激活的间隔作为传导时间即激活时间的指标。在梗死区,挥发性麻醉剂和I类抗心律不齐药物延长了梗死区的激活时间,而挥发性麻醉剂和I类抗心律不齐药物的组合显着延长了激活时间或阻止了延迟激活。在正常区域,观察到相似的协同相互作用,但是与梗死区域相比,这些药物的作用较小。从这些结果,讨论了解释协同相互作用的可能机制。

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