急性心筋虚血のsteady stateならびにtime-dependent slowing—lidocaineならびにverapamilの効果

Steady state and time-dependent slowing of conduction in acute myocardial ischemia:effect of lidocaine and verapamil

　心筋梗塞のごく初期に発生する心室性不整脈の発生機序としてreentryが提唱され^1,2,3），reentry発生の最も重要な因子として虚血部の伝導遅延（slow conduction）が考えられている^4）。伝導速度を決定するいくつかの因子のなかで細胞の脱分極速度（dv／dt）　maxは，最も重要であり^5），（dv／dt）　maxは静止膜電位の減少に伴うvoltage-dependentによる低下とtime-dependentにより低下することがsingle fiber studyにて明らかにされている^6,7）。このtime-dependentによる（dv／dt）　maxの低下は完全に再分極終了後から生じた早期収縮の（dv／dt）　maxの低下で，静止膜電位の減少に伴い一層著明になる。本研究では雑種成犬に急性心筋虚血を作成しsingle fiber studyで明らかにされたvoltage-dependentならびに　time-dependentによる伝導遅延が実際の虚血心筋においても認められることを明らかにし，さらに抗不整脈剤である　lidocaine,verapamilの伝導速度におよぼす影響を検討した。

To determine the steady state and time-depend-ent effects of verapamil and lidocaine on con-duction in acute myocardial ischemia, temporary (15min) ligations of the left anterior descending coronary artery were performed in 20 dogs. Sinus node was crushed and His pacing was performed at 2.5 beats/sec. Surface ECG, and bipolar elec-trograms in the ischemic and non-ischemic zones were recorded. Steady state effects were deter-mined by measuring intervals (H-EG) from the spikes of His pacing to the major deflections of electrograms recorded in ischemic and non-ischemic zones. To determine time-dependent effects, stimuli progressively decreased by 10 msec were introduced no earlier than the end of the T wave of the preceding beats. Control ligations were compared to those with verapamil and lido-caine. The changes were expressed as % increase from its own control value. In control ligation, the steady state H-EG interval in the ischemic zone was prolonged by 12.8±1.5% associated with slight time-dependent slowing (5.4±0.7%). These steady state and time-dependent effects were ex-aggerated by lidocain, but not verapamil. Thus, our results are pertinent to an understanding of arrhythmias associated with myocardial ischemia and the antiarrhythmic effects of lidocaine.