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Optogenetic Activation of Afferent Pathways in Brain Slices and Modulation of Responses by Volatile Anesthetics
Published on: July 23, 2020
Effects of volatile anesthetics on cardiac ion channels
R Hüneke1, J Fassl, R Rossaint
1Department of Anesthesiology, University Hospital, Rheinisch-Westfalische-Technische Hochschule (RWTH), Aachen, Germany.
Abstract:
The focus of the present review is on how interference with various ion channels in the heart may be the molecular basis for cardiac side-effects of gaseous anesthetics. Electrophysiological studies in isolated animal and human cardiomyocytes have identified the L-type Ca(2+) channel as a prominent target of anesthetics. Since this ion channel is of fundamental importance for the plateau phase of the cardiac action potential as well as for Ca(2+)-mediated electromechanical coupling, its inhibition may facilitate arrhythmias by shortening the refractory period and may decrease the contractile force. Effective inhibition of this ion channel has been shown for clinically used concentrations of halothane and, to a lesser extent, of isoflurane and sevoflurane, whereas xenon was without effect. Anesthetics furthermore inhibit several types of voltage-gated K(+) channels. Thereby, they may disturb the repolarization and bear a considerable risk for the induction of ventricular tachycardia in predisposed patients. In future, an advanced understanding of cardiac side-effects of anesthetics will derive from more detailed analyses of how and which channels are affected as well as from a better comprehension of how altered channel function influences heart function.
Insights
Gaseous anesthetics can cause heart problems by affecting ion channels. Inhibition of L-type Ca(2+) channels and K(+) channels by anesthetics may lead to arrhythmias and reduced heart contractility.
Area of Science:
- Cardiology
- Anesthesiology
- Molecular Biology
Background:
- Gaseous anesthetics are widely used in clinical practice.
- Cardiac side-effects associated with anesthetics necessitate understanding their molecular mechanisms.
- Ion channels play a crucial role in cardiac function and electrophysiology.
Purpose of the Study:
- To review the molecular basis of cardiac side-effects of gaseous anesthetics.
- To identify the specific ion channels targeted by anesthetics in the heart.
- To elucidate the functional consequences of anesthetic-induced ion channel modulation on cardiac activity.
Main Methods:
- Review of electrophysiological studies on isolated animal and human cardiomyocytes.
- Analysis of the effects of clinically used anesthetic concentrations on ion channel function.
- Correlation of altered ion channel function with cardiac electrophysiological parameters.
Main Results:
- L-type Ca(2+) channels are a prominent target, with inhibition affecting the action potential plateau and electromechanical coupling.
- Anesthetic inhibition of L-type Ca(2+) channels can decrease contractile force and facilitate arrhythmias.
- Voltage-gated K(+) channels are also inhibited, potentially disturbing repolarization and increasing the risk of ventricular tachycardia.
- Halothane showed effective inhibition, while isoflurane and sevoflurane had lesser effects; xenon was ineffective.
Conclusions:
- Interference with cardiac ion channels, particularly L-type Ca(2+) and voltage-gated K(+) channels, underlies the cardiac side-effects of gaseous anesthetics.
- Anesthetic-induced modulation of these channels can lead to arrhythmias and impaired cardiac contractility.
- Further research is needed to fully understand the complex interactions between anesthetics, ion channels, and cardiac function.
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