The Effects of Halothane, Isoflurane, and Sevoflurane on Ca2+ Current and Transient Outward K+ Current in Subendocardial and Subepicardial Myocytes from the Rat Left Ventricle

Rithalia, A; Hopkins, Philip M.; Harrison, Simon

doi:10.1213/01.ane.0000138422.40560.a9

Cited by 16 publications

(7 citation statements)

References 28 publications

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“…I to inactivation kinetics was also accelerated by halothane. Isoflurane also inhibited I to to a similar degree as halothane, but the effects of both anesthetics were evident only in rat subepicardial myocytes where the density of I to is greater than in the subendocardial myocytes [8]. Another volatile anesthetic, sevoflurane, had no effect on I to [8].…”

Section: Transient Outward Potassium Channelmentioning

confidence: 82%

“…Isoflurane also inhibited I to to a similar degree as halothane, but the effects of both anesthetics were evident only in rat subepicardial myocytes where the density of I to is greater than in the subendocardial myocytes [8]. Another volatile anesthetic, sevoflurane, had no effect on I to [8]. The differential effects of volatile anesthetics on the subepicardial and subendocardial myocytes can contribute to transmural effects on the cardiac action potential.…”

Section: Transient Outward Potassium Channelmentioning

confidence: 87%

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The yin and yang of volatile anesthetic action on cardiac potassium channels

Kwok

2005

International Congress Series

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Section: Transient Outward Potassium Channelmentioning

confidence: 82%

Section: Transient Outward Potassium Channelmentioning

confidence: 87%

The yin and yang of volatile anesthetic action on cardiac potassium channels

Kwok

2005

International Congress Series

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“…A solution containing halothane (Sigma) and isoflurane (Aerrane; Pharmacia Laboratories) was prepared from a 0.5 M stock solution made up in dimethyl sulfoxide (DMSO), as reported previously [21]. Solutions containing anesthetic were formulated with ≤0.12% dimethyl sulfoxide, a concentration that had no significant effect on calcium channel currents or on the electrical activity of the myocytes.…”

Section: Methodsmentioning

confidence: 99%

PKC independent inhibition of voltage gated calcium channels by volatile anesthetics in freshly isolated vascular myocytes from the aorta

et al. 2013

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In this study we used barium currents through voltage gated L-type calcium channels (recorded in freshly isolated cells with a conventional patch-clamp technique) to elucidate the cellular action mechanism for volatile anesthetics. It was found that halothane and isoflurane inhibited (dose-dependently and voltage independently) Ba2+ currents through voltage gated Ca2+ channels. Half maximal inhibitions occurred at 0.64 ± 0.07 mM and 0.86 ± 0.1 mM. The Hill slope value was 2 for both volatile anesthetics, suggesting the presence of more than one interaction site. Current inhibition by volatile anesthetics was prominent over the whole voltage range without changes in the peak of the current voltage relationship. Intracellular infusion of the GDPßS (100 μM) together with staurosporine (200 nM) did not prevent the inhibitory effect of volatile anesthetics. Unlike pharmacological Ca2+ channel blockers, volatile anesthetics blocked Ca2+ channel currents at resting membrane potentials. In other words, halothane and isoflurane induced an `initial block'. After the first 4 to 7 control pulses, the cells were left unstimulated and anesthetics were applied. The first depolarization after the pause evoked a Ca2+ channel current whose amplitude was reduced to 41 ± 3.4% and to 57 ± 4.2% of control values. In an analysis of the steady-state inactivation curve for voltage dependence, volatile anesthetics induced a negative shift of the 50% inactivation of the calcium channels. By contrast, the steepness factor characterizing the voltage sensitivity of the channels was unaffected. Unitary L-type Ca2+ channels blockade occurred under cell-attached configuration, suggesting a possible action of volatile anesthetics from within the intracellular space or from the part of the channel inside the lipid bilayer.

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“…Disturbance of the normal transmural dispersion of refractoriness is potentially arrhythmogenic. Using rat ventricular myocytes, halothane (0.1-3 mmol/L) and isoflurane (0.6 mmol/L) were shown to reduce I to amplitude, to shift steady-state inactivation to more negative potentials, and to accelerate inactivation rate of I to (Davies et al, 2000;Rithalia et al, 2004). Also, sevoflurane (≥0.3 mmol/L) accelerated the inactivation rate of Kv4.3/I to expressed in CHO cells (Kang et al, 2006).…”

Section: Other Cardiac K + Channels: Inward Rectifiers I To and Two-mentioning

confidence: 95%

Mechanisms Involved in Cardiac Sensitization by Volatile Anesthetics: General Applicability to Halogenated Hydrocarbons?

Himmel

2008

Critical Reviews in Toxicology

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An increased sensitivity of the heart to catecholamines or cardiac sensitization is a recognized risk during acute human exposure to halogenated hydrocarbons used as solvents, foam-blowing or fire-extinguishing agents, refrigerants, and aerosol propellants. Although cardiac sensitization to such "industrial" halocarbons can result in serious arrhythmia and death, research into its mechanistic basis has been limited, whereas the literature on volatile anesthetics (e.g., halothane, chloroform) is comparably extensive. A review of the literature on halocarbons and related volatile anesthetics was conducted. The available experimental evidence suggests that volatile anesthetics at physiologically relevant concentrations interact predominantly with the main repolarizing cardiac potassium channels hERG and I Ks , as well as with calcium and sodium channels at slightly higher concentrations. On the level of the heart, inhibition of these ion channels is prone to alter both action potential shape (triangulation) and electrical impulse conduction, which may facilitate arrhythmogenesis by volatile anesthetics per se and is potentiated by catecholamines. Action potential triangulation by regionally heterogeneous inhibition of calcium and potassium channels will facilitate catecholamine-induced afterdepolarizations, triggered activity, and enhanced automaticity. Inhibition of cardiac sodium channels will reduce conduction velocity and alter refractory period; this is potentiated by catecholamines and promotes reentry arrhythmias. Other cardiac and/or neuronal mechanisms might also contribute to arrhythmogenesis. The few scattered in vitro data available for halocarbons (e.g., FC-12, halon 1301, trichloroethylene) suggest inhibition of cardiac sodium (conduction), calcium and potassium channels (triangulation), extraneuronal catecholamine reuptake, and various neuronal ion channels. Therefore, it is hypothesized that halocarbons promote cardiac sensitization by similar mechanisms as volatile anesthetics. Experimental approaches for further investigation of these sensitization mechanisms by selected halocarbons are suggested.

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The Effects of Halothane, Isoflurane, and Sevoflurane on Ca2+ Current and Transient Outward K+ Current in Subendocardial and Subepicardial Myocytes from the Rat Left Ventricle

Cited by 16 publications

References 28 publications

The yin and yang of volatile anesthetic action on cardiac potassium channels

The yin and yang of volatile anesthetic action on cardiac potassium channels

PKC independent inhibition of voltage gated calcium channels by volatile anesthetics in freshly isolated vascular myocytes from the aorta

Mechanisms Involved in Cardiac Sensitization by Volatile Anesthetics: General Applicability to Halogenated Hydrocarbons?

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