Key result
Sevoflurane added to HTK solution increased total Cx43 levels and Cx43-pS368 levels, prevented conduction velocity slowing, and reduced reperfusion arrhythmias.
Why the study?
Whether the antiarrhythmic effect of sevoflurane against reperfusion ventricular arrhythmias is associated with connexin 43 protein had not been fully established.
Does sevoflurane added to HTK solution reduce reperfusion arrhythmias in isolated mouse hearts subjected to hypothermia and ischaemia?
Does sevoflurane added to HTK solution reduce reperfusion arrhythmias in isolated mouse hearts subjected to hypothermia and ischaemia?
Adding sevoflurane to HTK solution reduces reperfusion arrhythmias and myocardial injury in isolated mouse hearts, likely by preserving Cx43 phosphorylation and gap junction function.
Answers are grounded in this paper and cite their sources.
May warrant testing in human cardioplegia; hypothesis-generating for arrhythmia reduction in ischemia-reperfusion.
BACKGROUND: Reperfusion 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. METHODS: Hearts 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. RESULTS: Sevo-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. CONCLUSION: The 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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Li et al. (2019) studied Reperfusion ventricular arrhythmia associated with hypothermic ischaemic storage (n=16). Sevoflurane vs. HTK solution alone was evaluated on Total Cx43 level (p=<0.01). Sevoflurane added to HTK solution increased total Cx43 levels and Cx43-pS368 levels, prevented conduction velocity slowing, and reduced reperfusion arrhythmias.
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