Sevoflurane and cardioprotection

Siracusano, Luca; Girasole, Viviana; Piriou, Vincent; Mantz, Jean

doi:10.1093/bja/aem381

Cited by 4 publications

(1 citation statement)

References 13 publications

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“…133 Volatile anesthetics (sevoflurane, isoflurane, and desflurane) have, in several experimental and clinical settings, been shown to protect the heart from I/R injury. [134][135][136][137] Recently, isoflurane was demonstrated to have a similar effect on the rat liver, 138 and sevoflurane, in a prospective randomized study, protected the human liver from I/R injury during liver resection. 139 It is our practice to administer volatile anesthetics at least during the last 30 min before aortic cross clamping.…”

Section: Pulmonary Carementioning

confidence: 98%

Brain death and its implications for management of the potential organ donor

Bugge

2009

Acta Anaesthesiol Scand

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The systemic physiologic changes that occur during and after brain death affect all organs suitable for transplantation. Major changes occur in the cardiovascular, pulmonary, endocrine, and immunological systems, and, if untreated may soon result in cardiovascular collapse and somatic death. Understanding these complex physiologic changes is mandatory for developing effective strategies for donor resuscitation and management in such a way that the functional integrity of potentially transplantable organs is maintained. This review elucidates these physiological changes and their consequences, and based on these consequences the rationale behind current medical management of brain-dead organ donors is discussed.

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Section: Pulmonary Carementioning

confidence: 98%

Brain death and its implications for management of the potential organ donor

Bugge

2009

Acta Anaesthesiol Scand

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The cellular and molecular origin of reactive oxygen species generation during myocardial ischemia and reperfusion

Raedschelders

Ansley

Chen

2012

Pharmacology & Therapeutics

323

249

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Antiarrhythmic effect of sevoflurane as an additive to HTK solution on reperfusion arrhythmias induced by hypothermia and ischaemia is associated with the phosphorylation of connexin 43 at serine 368

Gao

et al. 2019

BMC Anesthesiol

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BackgroundReperfusion ventricular arrhythmia (RA) associated with hypothermic ischaemic storage is increasingly recognized as a substantial contributor to adverse consequences after heart transplantation. Ischemia- or hypothermia-induced gap junction (GJ) remodelling is closely linked to RA. Reducing GJ remodelling contributes to RA attenuation and is important in heart transplantation. However, sevoflurane has an antiarrhythmic effect associated with the connexin 43 (Cx43) protein that has not yet been fully established.MethodsHearts were divided into two groups according to a random number table: all hearts were arrested by an infusion of histidine-tryptophan-ketoglutarate (HTK) solution (4 °C) followed by (1) storage in HTK solution (4 °C) alone for 6 h (n = 8, Control group) or (2) storage in HTK solution supplemented with sevoflurane (2.5%) (4 °C) for 6 h (n = 8, Sevo-HTK group). First, the total Cx43 level and the phosphorylation of Cx43 at Ser368 (Cx43-pS368) were assessed by Western blotting, and the distribution of Cx43 was assessed by immunohistochemistry. Second, programmed electrical stimulation (PES) and monophasic action potential (MAP) recording were used to analyse the MAP duration (MAPD), conduction velocity (CV) and transmural repolarization dispersion (TDR). In addition, haematoxylin and eosin (HE) and terminal deoxynucleotidyl transferase-dUTP nick end labelling (TUNEL) staining were individually used to investigate the degree of myocardial pathological damage and cell apoptosis. Finally, bipolar electrograms were used to record the graft re-beating time and monitor RA during reperfusion for 15 to 30 min.ResultsSevo-HTK solution relatively increased the total Cx43 (P < 0.01) and Cx43-pS368 (P < 0.01) levels and prevented Cx43 redistribution (P < 0.05) and CV slowing (P < 0.001) but did not change TDR (P > 0.05). Additionally, the Cx43-pS368/total Cx43 ratio (P>0.05) was similar in the two groups. However, with Sevo-HTK solution, the graft re-beating times were shortened, myocardial pathological damage was ameliorated, and the number of apoptotic cells was markedly decreased.ConclusionThe reduction in hypothermia and ischaemia-induced reperfusion arrhythmias by the addition of sevoflurane to HTK solution may be related to the phosphorylation of Cx43 at serine 368.

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Sevoflurane and cardioprotection

Cited by 4 publications

References 13 publications

Brain death and its implications for management of the potential organ donor

Brain death and its implications for management of the potential organ donor

The cellular and molecular origin of reactive oxygen species generation during myocardial ischemia and reperfusion

Antiarrhythmic effect of sevoflurane as an additive to HTK solution on reperfusion arrhythmias induced by hypothermia and ischaemia is associated with the phosphorylation of connexin 43 at serine 368

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