2019
DOI: 10.1186/s12871-018-0656-8
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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

Abstract: 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 … Show more

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Cited by 9 publications
(4 citation statements)
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“…Previous studies in our group revealed that prolonged duration of repolarization and decreased CV of MAP form the electrophysiological basis of ventricular arrhythmias induced by hypothermic global ischemia reperfusion. 4,5 However, the changes in repolarization duration and CV of atrial myocardium with R-AAs were not observed. Kir2.1 and Cx40 proteins are closely related to atrial repolarization duration and CV, respectively.…”
Section: Discussionmentioning
confidence: 93%
See 1 more Smart Citation
“…Previous studies in our group revealed that prolonged duration of repolarization and decreased CV of MAP form the electrophysiological basis of ventricular arrhythmias induced by hypothermic global ischemia reperfusion. 4,5 However, the changes in repolarization duration and CV of atrial myocardium with R-AAs were not observed. Kir2.1 and Cx40 proteins are closely related to atrial repolarization duration and CV, respectively.…”
Section: Discussionmentioning
confidence: 93%
“…2 At present, research on reperfusion atrial arrhythmia (R-AA) is mainly focused on local ischemic myocardium. 2,3 Previous studies in our group have revealed that prolonged duration of repolarization and decreased conduction velocity (CV) form the electrophysiological basis of ventricular arrhythmias induced by hypothermic global ischemia-reperfusion (IR), 4,5 but that in atrial myocardium was not observed. Currently, changes in the duration of repolarization and CV in the atrial myocardium of hypothermic global IR atrial arrhythmia have not been reported.…”
Section: Introductionmentioning
confidence: 99%
“…22,23 Our previous research found that sevoflurane produced an antiarrhythmic effect by regulating the expression and location of Cx43 in the ventricle which improved electrophysiological stability after ischemia-reperfusion. 24,25 Moreover, cardiac fibroblasts culture medium containing sevoflurane increased the relative expression of Cx43 and enhanced cardiomyocyte activity following hypoxia/reoxygenation, but whether this is driven by exosomes is currently unknown. 26 Therefore, in this study, we hypothesized that sevoflurane would stabilize cardiac conduction and reduce the risk of RA by CFs-Exo.…”
Section: Introductionmentioning
confidence: 99%
“…Cx43 is subjected to lateralization and dephosphorylation during ischemia–reperfusion injury, thus leading to lateral conduction, formation of re-entry and electrical uncoupling thus triggering RA [ 10 , 11 ]. By observing myocardium with ischemia–RA, we found that the expression, distribution, and phosphatization states of Cx43 are all changed to different extents to reduce the conduction velocity of myocardium and increase the probability of formation of RA [ 12 ]; however, the specific correlation between Cx43 and miRNAs in hypothermic ischemia–RA has not been clarified.…”
Section: Introductionmentioning
confidence: 99%