Desflurane-induced post-conditioning against myocardial infarction is mediated by calcium-activated potassium channels: role of the mitochondrial permeability transition pore
British Journal of Anaesthesia, ISSN: 0007-0912, Vol: 108, Issue: 4, Page: 594-601
2012
- 21Citations
- 18Captures
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Metrics Details
- Citations21
- Citation Indexes21
- 21
- CrossRef16
- Captures18
- Readers18
- 18
Article Description
Desflurane (DES)-induced preconditioning is mediated by large-conductance calcium-activated potassium channels (BK Ca ). Whether BK Ca are involved in anaesthetic-induced post-conditioning is unknown. We tested the hypothesis that DES-induced post-conditioning is mediated by BK Ca upstream of the mitochondrial permeability transition pore (mPTP). Pentobarbital-anaesthetized male C57Black/6 mice were subjected to 45 min coronary artery occlusion (CAO) and 3 h reperfusion. Animals received either no intervention or dimethylsulphoxide (DMSO, 10 µl g –1 ). DES (1.0 MAC, 7.5 vol%) was administered for 18 min, starting 3 min before the end of CAO. The following agents were given either alone or in combination with DES: the BK Ca activator NS1619 (1 µg g −1 ), the BK Ca inhibitor iberiotoxin (IbTx, 0.05 µg g −1 ), the mPTP opener atractyloside (ATRA, 25 µg g −1 ), and the mPTP inhibitor cyclosporine A (CYC A, 10 µg g −1 ). Infarct size (IS) was determined with triphenyltetrazolium chloride and the area at risk with Evans Blue, respectively. IS in control animals was 48(6)%. Neither DMSO, IbTx nor ATRA affected myocardial IS. DES alone or NS1619 alone or the combination reduced IS ( P <0.05), CYC A alone or in combination with IbTx or DES also reduced IS ( P <0.05). DES-induced reduction of myocardial IS was completely abolished by IbTx and was partially blocked by ATRA and ATRA partially blocked IS reduction by NS1619. These data suggest that DES-induced post-conditioning against myocardial infarction is mediated by BK Ca and mPTP. Cardioprotection by BK Ca activator NS1619 might occur, at least in part, independently of mPTP.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S000709121732264X; http://dx.doi.org/10.1093/bja/aer496; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84865232636&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/22315330; https://linkinghub.elsevier.com/retrieve/pii/S000709121732264X; https://dx.doi.org/10.1093/bja/aer496
Elsevier BV
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