Potential effect of lidocaine on ischemic myocardial injury: experimental and clinical observations.
Potential effect of lidocaine on ischemic myocardial injury: experimental and clinical observations.
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利多卡因对缺血性心肌损伤的潜在作用：实验和临床观察。
DOI：
10.1016/0022-4804(78)90044-6
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发表时间：
1978
期刊：
影响因子：
--
通讯作者：
J. Vasko
中科院分区：
文献类型：
--
作者：
H. Boudoulas;P. Karayannacos;R. Lewis;G. Kakos;J. Kilman;J. Vasko
研究了利多卡因对急性心肌梗死（AMI）中缺血性心肌损伤的影响。对 20 只麻醉犬进行冠状动脉结扎术 (CAL)。狗被分为三组。 I 组 (n = 8) 仅接受 CAL，II 组 (n = 6) 在 CAL 后 30 分钟接受 3 mg/kg 利多卡因 (L)，III 组 (n = 6) 接受相同的 L 推注，并以 2 mg/min 的 L 输注 120 分钟。在 I 组中，ST 段抬高 (Σ ST) 总和以及通过心外膜标测测量的显示 >1 mV ST 抬高 (NST) 的部位数量在 CAL 后 30 至 150 分钟之间没有变化，平均 R 幅度显着下降，并记录了 12 个新 Q 波。在II组和III组中，L给药15分钟后，ΣST和NST显着下降（P<0.05），并且直到研究结束都保持不变。第 II 组和第 III 组之间的 Σ ST 和 NST 变化没有差异。在第 II 组和第 III 组中，CAL 后 30 至 150 分钟内未观察到 R 波幅度变化或 Q 波。 CAL后150分钟时，第二组冠状窦CPK比第一组增加更多（23±3 vs 49.7±9，P<0.05）。 L 推注后 5 分钟，peakdp/dt (510 ± 50 mm Hg/sec,P< 0.05) 和 dQ/dt (28 ± 2%,P< 0.05) 的降低证明了负性肌力作用。在 6 名前部 AMI 患者中研究了利多卡因对 Σ ST 和 NST 的影响。在所研究的患者中，L Σ ST 和 NST 均显着降低。这些数据表明利多卡因具有有益的作用，可以减少缺血性损伤和/或延缓缺血性坏死的过程。这似乎是由负性肌力作用引起的，这可能对心脏直视手术后早期和急性心肌梗塞患者有益。
The effect of lidocaine on ischemic myocardial injury was studied in acute myocardial infarction (AMI). In 20 anesthetized dogs coronary artery ligation (CAL) was performed. Dogs were divided into three groups. Group I (n= 8) had CAL only, Group II (n= 6) received 3 mg/kg of lidocaine (L) 30 min post-CAL, Group III (n= 6) received the same bolus injection of L and an L infusion of 2 mg/min for 120 min. In Group I the sum of ST segment elevation (Σ ST) and the number of sites showing >1 mV ST elevation (NST), as measured from epicardial mapping, were unchanged between 30 and 150 min post-CAL, the mean R magnitude decreased significantly, and 12 new Q waves were recorded. In Groups II and III, 15 min after L administration, Σ ST and NST decreased significantly (P< 0.05) and remained unchanged until the end of the study. There was no difference in Σ ST and NST changes between Groups II and III. No R wave magnitude changes or Q waves were observed between 30 and 150 min post-CAL in Groups II and III. Coronary sinus CPK at 150 min post-CAL increased more in Group II than in Group I (23 ± 3 vs 49.7 ± 9,P< 0.05). A negative inotropic effect was demonstrated by decreases in peakdp/dt(510 ± 50 mm Hg/sec,P< 0.05) anddQ/dt(28 ± 2%,P< 0.05) 5 min after the L bolus.This effect of lidocaine on Σ ST and NST was studied in six patients with anterior AMI. L decreased significantly both Σ ST and NST in the patients studied.These data suggest that lidocaine has a beneficial effect, decreasing ischemic injury and/or delaying the process of ischemic necrosis. This appears to be caused by a negative inotropic effect, which may be beneficial in the early post-open-heart surgery period and in patients with acute myocardial infarction.