Antagonistic Actions of Halothane and Sevoflurane on Spontaneous Ca2+Release in Rat Ventricular Myocytes

Graham, Mark; Hopkins, Philip M.; Harrison, Simon

doi:10.1097/00000542-200607000-00013

Cited by 10 publications

(3 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Enflurane, halothane, and isoflurane concentrations exceeding MAC by an order of magnitude minimally affect Ca ++ channels in vitro 96,97. Halothane and sevoflurane exert opposite effects on Ca ++ release from sarcoplasmic reticulum,98 but are nearly exactly additive in their capacities to produce immobility 16. Knockout of the α IG T-type calcium channel does not alter MAC in mice 99.…”

Section: Relevance Of Plausible Specific Targets (Alphabetical Order)mentioning

confidence: 99%

Is a New Paradigm Needed to Explain How Inhaled Anesthetics Produce Immobility?

Eger

Raines

Shafer³

et al. 2008

Anesthesia &Amp; Analgesia

View full text Add to dashboard Cite

A paradox arises from present information concerning the mechanism(s) by which inhaled anesthetics produce immobility in the face of noxious stimulation. Several findings, such as additivity, suggest a common site at which inhaled anesthetics act to produce immobility. However, two decades of focused investigation have not identified a ligand- or voltage-gated channel that alone is sufficient to mediate immobility. Indeed, most putative targets provide minimal or no mediation. For example, opioid, 5-HT3, gamma-aminobutyric acid type A and glutamate receptors, and potassium and calcium channels appear to be irrelevant or play only minor roles. Furthermore, no combination of actions on ligand- or voltage-gated channels seems sufficient. A few plausible targets (e.g., sodium channels) merit further study, but there remains the possibility that immobilization results from a nonspecific mechanism.

show abstract

Section: Relevance Of Plausible Specific Targets (Alphabetical Order)mentioning

confidence: 99%

Is a New Paradigm Needed to Explain How Inhaled Anesthetics Produce Immobility?

Eger

Raines

Shafer³

et al. 2008

Anesthesia &Amp; Analgesia

View full text Add to dashboard Cite

show abstract

“…Previous studies have also suggested that sevoflurane maintains SR Ca 2ϩ stores by blocking the spontaneous Ca 2ϩ release from the SR in rat ventricular myocytes. 49 It should be noted that sevoflurane exerts an inhibitory action on the plasma membrane Na ϩ /Ca 2ϩ exchanger 47 and Ca 2ϩ pump, 48 which could also result in Ca 2ϩ loading into the SR through the inhibition of Ca 2ϩ extrusion from the myocytes, 50 so long as there is sufficient adenosine 5Ј-triphosphate for SERCA-mediated SR Ca 2ϩ uptake. Because Ca 2ϩ depletion in the SR may act as an effective trigger for the activation of TRPC channels, [17][18][19] it is reasonable to propose that the better preservation of SR Ca 2ϩ levels by Postlong application of sevoflurane could result in less TRPC activation, and thereby contributes to a lower incidence of the Ca 2ϩ paradox, compared with Post application ( fig.…”

Section: Preservation Of Sr Ca 2؉ By Postlong Application Of Sevoflurmentioning

confidence: 99%

Sevoflurane Protects Ventricular Myocytes from Ca2+Paradox-mediated Ca2+Overload by Blocking the Activation of Transient Receptor Potential Canonical Channels

et al. 2011

View full text Add to dashboard Cite

show abstract

“…Importantly, in our cellular assay the mice were decapitated in the absence of anaesthesia because halothane has been described to alter calcium handling and increase spontaneous calcium release in rat ventricular myocytes (Graham et al . ), which could impair the cell isolation procedure and reduce cell viability and general health. After this, the heart was extracted and quickly immersed in a physiological saline solution, Cell Isolated Buffer (m m : 30 NaCl, 5.4 KCl, 0.5 MgCl 2 , 0.33 NaH 2 PO 4 , 25 Hepes and 22 glucose).…”

Section: Methodsmentioning

confidence: 99%

New insights into the elucidation of angiotensin‐(1–7) in vivo antiarrhythmic effects and its related cellular mechanisms

Joviano‐Santos

Santos‐Miranda

Joca

et al. 2016

Experimental Physiology

View full text Add to dashboard Cite

What is the central question of this study? Recently, there have been many studies exploring the biological effects of angiotensin-(1-7), which has been proved to have cardioprotective actions. However, the effects of this peptide on cardiac arrhythmias in vivo and details regarding its mechanism of action are still undetermined. What is the main finding and its importance? We investigated protective effects of angiotensin-(1-7) on cardiac arrhythmias in vivo, which were not properly explored in terms of cellular mechanisms. To verify effects of angiotensin-(1-7), we used different but complementary experimental approaches. Our data provide new evidence on the cellular mechanism and an in vivo demonstration of the acute antiarrhythmic effect of angiotensin-(1-7). Angiotensin-(1-7) [Ang-(1-7)] has been proved to have cardioprotective effects. However, the effects of this peptide on cardiac arrhythmias in vivo and details regarding its mechanism of action are still undetermined. The aim of this study was to investigate the protective effects of Ang-(1-7) against cardiac arrhythmias, its in vivo effects and cellular mechanism of action. We analysed the ECG upon inducement of arrhythmias in vivo in rats using a combination of halothane and adrenaline. To analyse the effects of Ang-(1-7) on cells, fresh mouse ventricular cardiomyocytes were isolated. The cardiomyocytes were superfused with a solution containing halothane and isoprenaline as a model to induce arrhythmias and used in three different approaches, namely a contractility assay, patch-clamp technique and confocal microscopy. The in vivo ECG showed that the injection of Ang-(1-7) (4 nm i.v.) significantly reduced cardiac arrhythmias [before, 49 ± 43 arrhythmic events versus after Ang-(1-7), 16 ± 14 arrhythmic events]. This effect was blocked by injection of A-779 and l-NAME, without changes in haemodynamic parameters. In addition, contractility experiments showed that Ang-(1-7) significantly decreased the number of arrhythmic events without changing the fractional shortening. This protection was associated with a reduction of the action potential repolarization and membrane hyperpolarization. Moreover, Ang-(1-7) decreased the number of calcium waves without any changes in the amplitude of the calcium transient, despite a significant reduction in the decay rate. Our data provide new evidence on the cellular mechanism together with an in vivo demonstration of the antiarrhythmic effects of Ang-(1-7).

show abstract

Antagonistic Actions of Halothane and Sevoflurane on Spontaneous Ca2+Release in Rat Ventricular Myocytes

Abstract: Application of halothane and removal of sevoflurane sensitize the SR Ca(2+) release process (and vice versa on removal). Sevoflurane reversed the effects of halothane, suggesting they may act at the same subcellular target on the SR.

Cited by 10 publications

References 27 publications

Is a New Paradigm Needed to Explain How Inhaled Anesthetics Produce Immobility?

Is a New Paradigm Needed to Explain How Inhaled Anesthetics Produce Immobility?

Sevoflurane Protects Ventricular Myocytes from Ca2+Paradox-mediated Ca2+Overload by Blocking the Activation of Transient Receptor Potential Canonical Channels

New insights into the elucidation of angiotensin‐(1–7) in vivo antiarrhythmic effects and its related cellular mechanisms

Contact Info

Product

Resources

About