Effects of Halothane and Enflurane on Conduction Velocity and Maximum Rate of Rise of Action Potential Upstroke in Guinea Pig Papillary Muscles

Ozaki, Suzuko; Nakaya, Haruaki; Gotoh, Yasuyuki; Azuma, Mitsue; Kemmotsu, Osamu; Kanno, Morio

doi:10.1213/00000539-198903000-00006

Cited by 20 publications

(16 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Least-squares analyses gave the slopes of 0.04 +-0.02. The slope values were far from the theoretical value of 1.0, which would be obtained if the square of the conduction velocity were decreased in proportion to the decrease in the V, , , as is the case by fast sodium channel blockers such as lidocaine (13).…”

Section: Resultscontrasting

confidence: 60%

“…Our recent study using conventional microelectrode techniques (13) has suggested that these volatile anesthetics impair the intraventricular conduction by mechanism(s) different from those involving fast sodium channel blockers such as lidocaine or tetrodotoxin. Both halothane and enflurane decrease conduction velocity with little influence on the maximum rate of rise of action potential upstroke (Vmax), whereas fast channel blockers (i.e., tetrodotoxin and lidocaine) decrease the square of the conduction velocity in proportion to the decrease in V, , , (13). These findings suggest that these volatile anesthetics might slow conduction, presumably by increasing the internal longitudinal resistance (i.e., by impairing cell-to-cell electrical coupling).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Effects of Isoflurane on Conduction Velocity and Maximum Rate of Rise of Action Potential Upstroke in Guinea Pig Papillary Muscles

Ozaki

Nakaya

Gotoh

et al. 1990

Anesthesia & Analgesia

Self Cite

View full text Add to dashboard Cite

This study was undertaken to determine whether isoflurane, a volatile anesthetic that is reported to possess a wide margin of cardiovascular safety, exerts electrophysiological effects on cardiac tissue. By use of standard microelectrode techniques, effects of isoflurane on the maximum rate of rise of action potential upstroke (Vmax) and conduction velocity were examined in guinea pig papillary muscles. Isoflurane decreased action potential amplitude and action potential duration in a concentration-dependent fashion. Isoflurane at 1.5 and 2.0 MAC decreased conduction velocity with as little influence on the maximum rate of rise of action potential upstroke as that exerted by halothane and enflurane. However, the effect of isoflurane in slowing intraventricular conduction was less than that of halothane and enflurane when compared at equi-MAC concentrations. Thus, isoflurane may be a safer anesthetic for the patients with intraventricular conduction abnormalities.

show abstract

Section: Resultscontrasting

confidence: 60%

mentioning

confidence: 99%

Effects of Isoflurane on Conduction Velocity and Maximum Rate of Rise of Action Potential Upstroke in Guinea Pig Papillary Muscles

Ozaki

Nakaya

Gotoh

et al. 1990

Anesthesia & Analgesia

Self Cite

View full text Add to dashboard Cite

show abstract

“…On the other hand, Terrar and Victory [18] showed that halothane inhibits cell-to-cell electrical coupling. In addition, Ozaki et al [19], reported that halothane and enflurane reduced the conduction velocity in guinea pig papillary muscles without any significant reduction of Vmax. Spray and Burt [20] showed that a variety of lipophilic molecules, including halothane, and myoplasmic acidification reduce cell-to-cell electrical coupling.…”

Section: Discussionmentioning

confidence: 97%

Electrophysiologic effects of volatile anesthetics, sevoflurane and halothane, in a canine myocardial infarction model

et al. 1994

View full text Add to dashboard Cite

The effects of sevoflurane and halothane on the effective refractory period (ERP) and ventricular activation were examined in a canine myocardial infarction model. Sevoflurane (1 MAC) reduced the heart rate and prolonged ERP in both normal and infarcted zones. A prolongation of ERP with sevoflurane was observed also during atrial pacing at a fixed rate, but the effect was less than during sinus rhythm. Sevoflurane either further delayed or blocked the delayed activation entirely in the infarcted zones with only slight effects on the activation of the normal zones. Halothane (1 MAC) prolonged ERP during sinus rhythm and atrial pacing, but to a lesser extent during the latter. Halothane also depressed ventricular activation in the infarcted zone during atrial pacing. In conclusion, sevoflurane as well as halothane selectively depresed the delayed activation and the prolongation of ERP in myocardial infarction, which may inhibit ventricular arrhythmias in myocardial infarction.

show abstract

“…Sevoflurane and isoflurane may have similar effects, which may cause a selective depression of delayed conduction in the infarcted zone. However, several inves tigators suggested that mechanisms of the effects of the volatile anesthetics and class I antiarrhythmic drugs on ventricular conduction may be different (10,17,18). Ozaki et al reported that halothane and enflurane depressed the conduction velocity without depressing vmax in isolated guinea pig papillary muscle (10).…”

Section: Discussionmentioning

confidence: 99%

“…They showed that halothane decreased the maximal rate of depolarization (Vm3, slowed the conduction and prolonged the effective refrac tory period in the infarcted zones. On the other hand, Ozaki et al reported that volatile anesthetics such as halothane or enflurane slowed ventricular conduction without any significant depression of Vmax in isolated guinea pig papillary muscle (10). It is well known that ven tricular delayed conduction in infarcted myocardium plays an important role in the occurrence of reentrant ven tricular arrhythmias and that class I antiarrhythmic drugs cause their antiarrhythmic actions partly by a block of the delayed conduction (11).…”

mentioning

confidence: 99%

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

View full text Add to dashboard Cite

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.

show abstract

Effects of Halothane and Enflurane on Conduction Velocity and Maximum Rate of Rise of Action Potential Upstroke in Guinea Pig Papillary Muscles

Cited by 20 publications

References 0 publications

Effects of Isoflurane on Conduction Velocity and Maximum Rate of Rise of Action Potential Upstroke in Guinea Pig Papillary Muscles

Effects of Isoflurane on Conduction Velocity and Maximum Rate of Rise of Action Potential Upstroke in Guinea Pig Papillary Muscles

Electrophysiologic effects of volatile anesthetics, sevoflurane and halothane, 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

Contact Info

Product

Resources

About