Lidocaine abolishes the myocardial protective effect of sevoflurane post‐conditioning

Yan, Min; Chen, C; Zhang, F; Chen, G

doi:10.1111/j.1399-6576.2007.01487.x

Cited by 13 publications

(12 citation statements)

References 29 publications

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“…Sevoflurane, a volatile anesthetic, was demonstrated to have cardioprotective effect in ischemic and reperfused rat hearts by postconditioning (Obal et al, 2005;. Obal et al(2005) has elucidated that the adenosine triphosphate-sensitive potassium (K ATP ) channel did involve the postconditioning of sevoflurane, which was in line with our previous results (Yan et al, 2008). Nevertheless, it might not be the only mediator underlying the complicating pathological lesion (Zhao and Vinten-Johansen, 2006).…”

Section: Introductionsupporting

confidence: 78%

Postconditioning of sevoflurane and propofol is associated with mitochondrial permeability transition pore

Zhang

Wang

et al. 2008

J. Zhejiang Univ. Sci. B

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Section: Introductionsupporting

confidence: 78%

Postconditioning of sevoflurane and propofol is associated with mitochondrial permeability transition pore

Zhang

Wang

et al. 2008

J. Zhejiang Univ. Sci. B

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“…Moreover, administration of isoflurane immediately before and during early reperfusion after prolonged ischemia protected the myocardium against infarction (Shim et al, 2007). Recently, experimental sevoflurane postconditioning improved postischemic recovery and reduced myocardial infarct size (Yan et al, 2008). Sevoflurane postconditioning possesses a strong antiarrhythmic effect against reperfusion-induced ventricular fibrillation by conversion of ventricular fibrillation into regular rhythm (Zhang et al, 2009).…”

Section: Anesthetic Postconditioningmentioning

confidence: 99%

Myocardial postconditioning: Next step to cardioprotection

Rohilla¹,

Rohilla

Kushnoor

2011

Arch. Pharm. Res.

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Myocardial ischemia is a condition in which lack of blood flow to the cardiac muscle occurs resulting in deficient oxygen and nutrient supply to the heart. The restoration of blood flow to an organ or tissue is termed reperfusion. Brief episodes of ischemia and reperfusion given after prolonged ischemia and at the onset of reperfusion denotes postconditioning. Myocardial postconditioning is a phenomenon in which myocardium from lethal ischemia-reperfusion injury is protected. However, numerous experimental studies reveal that the cardioprotective effects of postconditioning are suppressed in various pathological states. This review critically discusses the mechanisms involved in the cardioprotective effects of postconditioning and factors affecting the cardioprotective potential of myocardial postconditioning.

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“…The group of Schlack firstly reported that lidocaine, a potent inhibitor not only of sodium channels but also of ATP-sensitive potassium channels, blocked (at supratherapeutic concentrations) cardioprotection induced by ischaemic preconditioning in isolated rat hearts [53]. This effect has been recently recapitulated for sevoflurane postconditioning under the same experimental conditions [54]. Similarly, the former group reported that ketamine completely abolished the IPreC-related cardioprotection both in vitro [55] and in vivo [56], an effect that was stereospecific for the R (À) enantiomer.…”

Section: Cardioprotection Attenuation/blockadementioning

confidence: 87%

Volatile anaesthetics and cardioprotection – lessons from animal studies

Muntean

Ordodi

Ferrera

et al. 2012

Fundamemntal Clinical Pharma

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Volatile anaesthetics emerged as important cardioprotective agents in both animal models of ischaemia/reperfusion injury and humans with coronary artery disease. Their administration before a prolonged ischaemic episode is known as anaesthetic preconditioning, whereas when given at the very onset of reperfusion, the strategy is termed anaesthetic postconditioning. Both types of anaesthetic conditioning reduce, albeit not to the same degree, the extent of myocardial injury. They share similar, albeit not identical, intracellular signal transduction pathways with their widely investigated counterparts, ischaemic pre- and postconditioning. Despite a wealth of preclinical evidence for cardioprotection for anaesthetic conditioning strategies, their translation into clinical therapy has been rather disappointing. This review highlights the major findings on the cardioprotective effects of volatile anaesthetics in experimental settings. It explores hypotheses that may explain the lack of efficacy observed in several past clinical studies paving the way for future preclinical and translational studies.

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Lidocaine abolishes the myocardial protective effect of sevoflurane post‐conditioning

Abstract: Sevourane-induced post-conditioning effectively protected myocardium against reperfusion damage and its cytoprotection was reversed by 20 microg/ml lidocaine.

Cited by 13 publications

References 29 publications

Postconditioning of sevoflurane and propofol is associated with mitochondrial permeability transition pore

Postconditioning of sevoflurane and propofol is associated with mitochondrial permeability transition pore

Myocardial postconditioning: Next step to cardioprotection

Volatile anaesthetics and cardioprotection – lessons from animal studies

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