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冠状动脉内注射乙醇或苯酚可消除乌头碱诱发的犬室性心动过速。

Intracoronary ethyl alcohol or phenol injection ablates aconitine-induced ventricular tachycardia in dogs.

作者信息

Inoue H, Waller B F, Zipes D P

机构信息

Krannert Institute of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis 46202.

出版信息

J Am Coll Cardiol. 1987 Dec;10(6):1342-9. doi: 10.1016/s0735-1097(87)80139-0.

DOI:10.1016/s0735-1097(87)80139-0
PMID:3680803
Abstract

The hypothesis whether localized ventricular tachycardia could be ablated by myocardial necrosis induced with chemical agents injected into a coronary artery was tested. In 59 anesthetized dogs, a diagonal branch of the left anterior descending coronary artery was cannulated either occlusively or nonocclusively. Localized ventricular tachycardia was induced by injecting approximately 0.01 ml of 30 micrograms/ml of aconitine solution into the left ventricular wall perfused by the cannulated diagonal branch in 54 dogs. In eight untreated control dogs, aconitine-induced ventricular tachycardia lasted 10.2 +/- 2.3 minutes or degenerated into ventricular fibrillation after 7.0 +/- 4.0 minutes. In the remaining 46 dogs, 1 ml of saline solution, 25, 50 or 100% ethyl alcohol or 0.94 ml (mean [range 0.4 to 2.0]) of 25% phenol at room temperature was injected into the occluded coronary artery and 1 ml of 100% ethyl alcohol at body temperature was injected into the nonoccluded coronary artery. Ventricular tachycardia was eliminated in 9 (82%) of 11 dogs receiving phenol, 7 (88%) of 8 dogs receiving 100% ethyl alcohol occlusively, 6 (75%) of 8 dogs receiving 100% ethyl alcohol nonocclusively and 6 (67%) of 9 dogs receiving 50% ethyl alcohol for an entire follow-up period of 10 to 60 minutes. However, saline solution and 25% ethyl alcohol suppressed ventricular tachycardia only transiently in 8 (53%) of 15 and 3 (60%) of 5 dogs, respectively. Left ventricular end-diastolic pressure rose from 8.0 to 11.2 mm Hg (p less than 0.05) immediately after injection of 100% ethyl alcohol in seven dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

对冠状动脉内注射化学药剂诱发心肌坏死能否消融局部室性心动过速这一假说进行了验证。在59只麻醉犬中,对左前降支冠状动脉的一个对角支进行闭塞或非闭塞插管。在54只犬中,通过向由插管对角支灌注的左心室壁注射约0.01 ml 30微克/毫升的乌头碱溶液诱发局部室性心动过速。在8只未治疗的对照犬中,乌头碱诱发的室性心动过速持续10.2±2.3分钟,或在7.0±4.0分钟后恶化为心室颤动。在其余46只犬中,向闭塞冠状动脉内注射1 ml生理盐水、25%、50%或100%乙醇或0.94 ml(平均[范围0.4至2.0])室温下的25%苯酚,并向非闭塞冠状动脉内注射1 ml体温下的100%乙醇。在接受苯酚治疗的11只犬中有9只(82%)、闭塞接受100%乙醇治疗的8只犬中有7只(88%)、非闭塞接受100%乙醇治疗的8只犬中有6只(75%)以及接受50%乙醇治疗的9只犬中有6只(67%)在整个10至60分钟的随访期内心室性心动过速被消除。然而,生理盐水和25%乙醇分别仅使15只犬中的8只(53%)和5只犬中的3只(60%)的室性心动过速得到短暂抑制。在7只犬注射100%乙醇后,左心室舒张末期压力立即从8.0毫米汞柱升至11.2毫米汞柱(p<0.05)。(摘要截取自250字)

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