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本文引用的文献

1
Mechanism of the myocardial effects of bretylium.溴苄铵对心肌作用的机制。
Circ Res. 1962 Mar;10:347-53. doi: 10.1161/01.res.10.3.347.
2
Kinetics of antifibrillatory effects of bretylium: correlation with myocardial drug concentrations.溴苄铵抗纤颤作用的动力学:与心肌药物浓度的相关性
Am J Cardiol. 1980 Oct;46(4):583-92. doi: 10.1016/0002-9149(80)90507-x.
3
Decoupling of heart muscle cells: correlation with increased cytoplasmic calcium activity and with changes of nexus ultrastructure.心肌细胞解耦联:与细胞质钙活性增加及连接子超微结构变化的相关性。
J Membr Biol. 1980 Mar 31;53(1):63-75. doi: 10.1007/BF01871173.
4
Effects of duration of ventricular fibrillation and heart massage on haemodynamic responses after defibrillation in dogs.心室颤动持续时间和心脏按摩对犬除颤后血流动力学反应的影响。
Cardiovasc Res. 1983 May;17(5):282-9. doi: 10.1093/cvr/17.5.282.
5
Class III action of beta-blocking agents.β受体阻滞剂的III类作用。
Cardiovasc Res. 1984 Nov;18(11):683-9. doi: 10.1093/cvr/18.11.683.
6
A classification of antiarrhythmic actions reassessed after a decade of new drugs.在十年新药研发之后重新评估的抗心律失常作用分类。
J Clin Pharmacol. 1984 Apr;24(4):129-47. doi: 10.1002/j.1552-4604.1984.tb01822.x.
7
Effects of propranolol on the transmembrane potentials of ventricular muscle and Purkinje fibers of the dog.普萘洛尔对犬心室肌和浦肯野纤维跨膜电位的影响。
Circ Res. 1968 May;22(5):661-77. doi: 10.1161/01.res.22.5.661.
8
The effect of bretylium tosylate on the electrophysiologic properties of ventricular muscle and Purkinje fibers.甲苯磺丁苄胺对心室肌和浦肯野纤维电生理特性的影响。
Am J Cardiol. 1971 Jan;27(1):82-92. doi: 10.1016/0002-9149(71)90086-5.
9
Effect of altering potassium concentration on the action of lidocaine and diphenylhydantoin on rabbit atrial and ventricular muscle.改变钾离子浓度对利多卡因和苯妥英钠作用于兔心房和心室肌的影响。
Circ Res. 1971 Sep;29(3):286-95. doi: 10.1161/01.res.29.3.286.
10
A fourth class of anti-dysrhythmic action? Effect of verapamil on ouabain toxicity, on atrial and ventricular intracellular potentials, and on other features of cardiac function.第四类抗心律失常作用?维拉帕米对哇巴因毒性、心房和心室细胞内电位以及心脏功能其他特征的影响。
Cardiovasc Res. 1972 Mar;6(2):109-19. doi: 10.1093/cvr/6.2.109.

已确立的心室颤动的药理学分析。

Pharmacological analysis of established ventricular fibrillation.

作者信息

Carlisle E J, Allen J D, Kernohan W G, Leahey W, Adgey A A

机构信息

Department of Physiology, Queen's University, Belfast, Northern Ireland.

出版信息

Br J Pharmacol. 1990 Jul;100(3):530-4. doi: 10.1111/j.1476-5381.1990.tb15841.x.

DOI:10.1111/j.1476-5381.1990.tb15841.x
PMID:2167735
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1917813/
Abstract
  1. The effects of anti-arrhythmic drugs on the power spectrum of established ventricular fibrillation induced by endocardial electrical stimulation, have been studied in greyhounds anaesthetized with sodium pentobarbitone (35 mg kg-1, i.v.). 2. In dogs receiving no drug, initial recording of ventricular fibrillation showed a dominant frequency of 9.9 +/- 0.7 Hz (lead II) and 10.0 +/- 0.6 Hz (endocardium). After 3.3 min the frequency had fallen to 4.0 +/- 0.4 Hz in lead II, but remained high in the endocardium (10.7 +/- 0.5 Hz). 3. Lignocaine significantly reduced the dominant frequency for fibrillation recorded from lead II at (0-80 s), and for endocardial fibrillation at (0-200 s). 4. Pretreatment with propranolol or bretylium had little effect on the time course of the dominant frequency of fibrillation in lead II or the endocardium. 5. Verapamil prevented the fall in frequency seen in lead II after 80 s in the no drug group. A significantly higher frequency was maintained in both lead II (14.7 +/- 0.9 Hz) and the endocardium (14.8 +/- 0.9 Hz) for 3.3 min, compared with the no drug group (P less than 0.01). 6. Activation of fast sodium channels may determine the rapid frequency of the initial stages of ventricular fibrillation. The rapid fall in dominant frequency in lead II after fibrillation for 80 s can be prevented by calcium channel blockade and may be due to intracellular accumulation of calcium.
摘要
  1. 研究了抗心律失常药物对戊巴比妥钠(35mg/kg,静脉注射)麻醉的灵缇犬心内膜电刺激诱发的持续性室颤功率谱的影响。2. 在未用药的犬中,室颤初始记录显示II导联的主导频率为9.9±0.7Hz,心内膜为10.0±0.6Hz。3.3分钟后,II导联频率降至4.0±0.4Hz,但心内膜频率仍较高(10.7±0.5Hz)。3. 利多卡因显著降低了II导联(0 - 80秒)和心内膜(0 - 200秒)记录的室颤主导频率。4. 普萘洛尔或溴苄铵预处理对II导联或心内膜室颤主导频率的时间进程影响不大。5. 维拉帕米阻止了未用药组80秒后II导联出现的频率下降。与未用药组相比,II导联(14.7±0.9Hz)和心内膜(14.8±0.9Hz)在3.3分钟内维持了显著更高的频率(P<0.01)。6. 快速钠通道的激活可能决定室颤初始阶段的快速频率。室颤80秒后II导联主导频率的快速下降可通过钙通道阻滞来预防,这可能是由于细胞内钙的蓄积。