Clinical Use of Antiarrhythmic Drugs

Bigger, J. Thomas; Heissenbuttel, Robert H.

doi:10.1080/00325481.1970.11698101

Cited by 22 publications

(13 citation statements)

References 20 publications

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“…The present study showed that volatile anesthetics and class I antiarrhythmic drugs depressed the delayed activa tion in infarcted zones of canine ventricles, which is con sistent with previous results (5,15,16). In the present study, the effects of sevoflurane and isoflurane were exam ined, because these are now frequently used.…”

Section: Discussionsupporting

confidence: 63%

“…Bentley et al reported that halothane decreased the clearance of lidocaine mainly by a decreased hepatic blood flow and/or inhibition of hepatic lidocaine metabolism (23). Although the effects of sevoflurane or isoflurane on hepatic biotransformation may be to a less extent compared to those of halothane (27,28), the syner gistic interaction between the volatile anesthetics and lidocaine observed in the present study may be caused partly by a decrease in the hepatic metabolism of lidocaine through a reduction of hepatic blood flow, because hepatic metabolism largely contributes to the clearance of lidocaine (15). However, a synergistic inter action in the depressant effect on the activation time was similarly observed between the volatile anesthetics and procainamide, in spite of the fact that hepatic metabolism of procainamide occurs to a less extent comapared to that of lidocaine (15).…”

Section: Discussionmentioning

confidence: 58%

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Electrophysiologic Interaction between Class I Antiarrhythmic Drugs and Volatile Anesthetics in Depressant Effects on Ventricular Activation in a Canine Myocardial Infarction Model

Hashimoto

Imamura

Ikeda

et al. 1994

Japanese Journal of Pharmacology

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ABSTRACT-Previous studies showed that volatile anesthetics depressed ventricular delayed activation in a canine myocardial infarction model. It is well known that class I antiarryhthmic drugs depress the ven tricular activation in the infarcted myocardium. In the present study, we examined the electrophysiologic interaction between volatile anesthetics (sevoflurane, isoflurane) and class I antiarrhythmic drugs (lidocaine, procainamide) in effects on the ventricular delayed activation in a canine myocardial infarction model. The conduction time of the premature stimulation-induced ventricular excitation was measured in both normal and infarcted zones of the ventricle. An interval from the premature stimulus artifact to the epicardial ac tivation was measured on bipolar electrograms as an index of conduction time, i.e., activation time. In the infarcted zone, the volatile anesthetics and class I antiarrhythmic drugs prolonged the activation time in the infarcted zone, and the combination of the volatile anesthetics and the class I antiarrhythmic drugs mark edly prolonged the activation time or blocked the delayed activation. In the normal zone, a similar synergistic interaction was observed, but the effect of these drugs was less compared with that in the infarcted zone. From these results, possible mechanisms to explain the synergistic interaction were discussed.

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Section: Discussionsupporting

confidence: 63%

Section: Discussionmentioning

confidence: 58%

Electrophysiologic Interaction between Class I Antiarrhythmic Drugs and Volatile Anesthetics in Depressant Effects on Ventricular Activation in a Canine Myocardial Infarction Model

Hashimoto

Imamura

Ikeda

et al. 1994

Japanese Journal of Pharmacology

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“…Although there are no published randomized trials of lidocaine in humans, anecdotal reports support its use in DCS (12). A sodium channel blocker, lidocaine has been used as a local anes thetic and prophylactic antiarrhythmic agent for ven tricular tachycardia and fibrillation (4). It readily crosses the blood-brain barrier (43), has a high volume of distri bution, and is rapidly metabolized by the liver.…”

Section: Lidocainementioning

confidence: 99%

Pharmacological Interventions to Decompression Sickness in Rats: Comparison of Five Agents

Montcalm-Smith¹,

Fahlman²,

Kayar³

2008

asem

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“…However, the autonomic effects of several other antiarrhythmic drugs are undesirable. Noradrenaline release and adrenergic neuronal blockade by bretylium, a-adrenoceptor blockade by quinidine and the anticholinergic activity ofquinidine and disopyramide limit the clinical usefulness of these agents (Bigger & Hoffman, 1980). Changrolin, a novel class I antiarrhythmic agent (Xu & Carmeliet, 1981) used in the Peoples Republic ofChina (Xu & Qu, 1978: Li et al, 1979, has also been reported to possess parasympatholytic activity in vivo (Chen et al, 1979).…”

Section: Introductionmentioning

confidence: 99%

Comparison of the parasympatholytic activity of ACC‐9358 and disopyramide

Brown¹,

Gorczynski²,

Reynolds³

et al. 1986

British J Pharmacology

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ACC‐9358 (N‐[(3,5‐di(pyrrolidinylmethyl)‐4‐hydroxy)benzoyl]aniline) is a newly developed analogue of changrolin, an antiarrhythmic agent used in the Peoples Republic of China. Since changrolin and other antiarrhythmic agents exert parasympatholytic activity which may limit their clinical usefulness, it was of interest to examine the parasympatholytic effects of ACC‐9358. For comparative purposes we also studied the parasympatholytic activity of disopyramide. In guinea‐pig isolated ileal strips, disopyramide, 3–30 μM, and ACC‐9358, 100–300 μM, competitively antagonized carbachol‐induced contractions with pA2 values of 5.78 and 4.17, respectively. In guinea‐pig isolated right atria, disopyramide 3–30 μM, competitively antagonized methacholine‐induced slowing of spontaneous beating with a pA2 value of 5.99 whereas ACC‐9358, 3–300 μM, produced no significant muscarinic blockade in this preparation. Disopyramide (1.9–15 mg kg−1, i.v.), but not ACC‐9358 (7.5‐1.5 mg kg−1, i.v.), significantly increased rat pupil diameter in vivo. Disopyramide and ACC‐9358 blocked vagal‐induced reductions in heart rate in dogs anaesthetized with pentobarbitone. ED50 values were approximately 0.65 and 11.25 mg kg−1, respectively. We conclude that ACC‐9358 possesses significantly less parasympatholytic activity than disopyramide.

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Clinical Use of Antiarrhythmic Drugs

Cited by 22 publications

References 20 publications

Electrophysiologic Interaction between Class I Antiarrhythmic Drugs and Volatile Anesthetics in Depressant Effects on Ventricular Activation in a Canine Myocardial Infarction Model

Electrophysiologic Interaction between Class I Antiarrhythmic Drugs and Volatile Anesthetics in Depressant Effects on Ventricular Activation in a Canine Myocardial Infarction Model

Pharmacological Interventions to Decompression Sickness in Rats: Comparison of Five Agents

Comparison of the parasympatholytic activity of ACC‐9358 and disopyramide

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