Nakaya H, Hattori Y, Kanno M
Jpn J Pharmacol. 1980 Oct;30(5):587-97. doi: 10.1254/jjp.30.587.
Effects of calcium antagonists and lidocaine on the conduction delay observed in the ischemic myocardium were studied in 24 open-chest anesthetized dogs. Acute myocardial ischemia was produced by complete occlusion of the left anterior descending coronary artery (LAD) for 5 to 10 minutes. The conduction time was measured from the initial deflection of V waves on the His bundle electrograms to the major deflection of the bipolar electrograms recorded from the ischemic and non-ischemic subepicardium under a constant atrial pacing. LAD occlusion produced conduction delay in the ischemic zone (14.3 +/- 2.3 msec, p less than 0.001) with no effect on the normal zone. This ischemia-induced conduction delay was reversible and rate-dependently increased. Administration of lidocaine (2 mg/kg bolus, 4.3 mg/kg/hr constant infusion) prior to the second occlusion increased conduction delay by 12.9 +/- 1.9 msec (p less than 0.001) whereas diltiazem (0.4 mg/kg i.v.) and verapamil (0.3 mg/kg i.v.) reduced the ischemia-induced conduction delay by 12.7 +/- 4.9 msec (p less than 0.05) and 8.4 +/- 1.8 msec (p less than 0.001), respectively. These results indicate that slow channel blocking agents reduce the conduction delay induced by the myocardial ischemia, in contrast with the prolonging effect of lidocaine.
在24只开胸麻醉犬中研究了钙拮抗剂和利多卡因对缺血心肌中观察到的传导延迟的影响。通过完全闭塞左冠状动脉前降支(LAD)5至10分钟产生急性心肌缺血。在恒定心房起搏下,测量从希氏束电图上V波的初始偏转至缺血和非缺血心外膜下记录的双极电图的主要偏转的传导时间。LAD闭塞在缺血区产生传导延迟(14.3±2.3毫秒,p<0.001),而对正常区无影响。这种缺血诱导的传导延迟是可逆的且呈速率依赖性增加。在第二次闭塞前给予利多卡因(2mg/kg推注,4.3mg/kg/hr持续输注)使传导延迟增加12.9±1.9毫秒(p<0.001),而地尔硫卓(0.4mg/kg静脉注射)和维拉帕米(0.3mg/kg静脉注射)分别使缺血诱导的传导延迟减少12.7±4.9毫秒(p<0.05)和8.4±1.8毫秒(p<0.001)。这些结果表明,与利多卡因的延长作用相反,慢通道阻滞剂可减少心肌缺血诱导产生的传导延迟。