Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 김현수 | - |
dc.date.accessioned | 2017-01-05T02:01:42Z | - |
dc.date.available | 2017-01-05T02:01:42Z | - |
dc.date.issued | 2012 | - |
dc.identifier.issn | 0022-4804 | - |
dc.identifier.other | OAK-8668 | - |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/233438 | - |
dc.description.abstract | Background: Hyperglycemia attenuates cardioprotection by remifentanil-preconditioning in ischemia-reperfusion in vivo in diabetic rats. However, the effects of hyperglycemia in cultured ventricular myocytes remains unknown. Therefore, we examined the in vitro effects of hyperglycemia on hypoxia-reoxygenation (H/R) and cardioprotection from remifentanil- preconditioning in isolated neonatal rat ventricular myocytes (NRVMs), including effects on apoptotic signaling pathways and Ca 2+ homeostasis. Materials and Methods: NRVMs were cultured in medium with 5.5 mM (normoglycemia) or 25.5 mM glucose for one day. Then, NRVMs in H/R groups were exposed to 1 h of hypoxia and 5 h of reoxygenation with or without remifentanil-preconditioning at 1 μM. Cell viability, apoptosis, and Ca 2+ homeostasis were assessed by MTT assay, caspase-3 assay, confocal microscopy and immunoblots. Results: In normoglycemia, remifentanil-preconditioning improved the viability of cardiomyocytes (P < 0.01) and prevented the increase of caspase-3 activity and Ca 2+ overload after H/R injury (P < 0.05). In addition, decrease in Akt, ERK1/2, and Bcl-2, and the increase in Bax by H/R was attenuated by remifentanil-preconditioning (P < 0.05). However, in hyperglycemia, the viability was partially impaired after H/R but not improved by remifentanil-preconditioning. Apoptotic activity, Ca 2+ concentration, and apoptotic kinases except Akt were not affected by either H/R or remifentanil-preconditioning under hyperglycemia. Akt phosphorylation was decreased by H/R but not restored by remifentanil preconditioning. Conclusions: Remifentanil preconditioning under normoglycemia renders NRVMs resistant to H/R injury by reducing apoptosis and intracellular Ca 2+ concentrations. The mechanism appears to be modulation of apoptotic signaling. However, hyperglycemia mitigates H/R injury in NRVMs, and may reduce the protective effect of remifentanil-preconditioning that may be associated with the Akt pathways. © 2012 Elsevier Inc. All rights reserved. | - |
dc.language | English | - |
dc.title | Hyperglycemia attenuates myocardial preconditioning of remifentanil | - |
dc.type | Article | - |
dc.relation.issue | 2 | - |
dc.relation.volume | 174 | - |
dc.relation.index | SCI | - |
dc.relation.index | SCIE | - |
dc.relation.index | SCOPUS | - |
dc.relation.startpage | 231 | - |
dc.relation.lastpage | 237 | - |
dc.relation.journaltitle | Journal of Surgical Research | - |
dc.identifier.doi | 10.1016/j.jss.2011.01.018 | - |
dc.identifier.wosid | WOS:000302777500016 | - |
dc.identifier.scopusid | 2-s2.0-84859518270 | - |
dc.author.google | Kim H.S. | - |
dc.author.google | Kim S.Y. | - |
dc.author.google | Kwak Y.L. | - |
dc.author.google | Hwang K.C. | - |
dc.author.google | Shim Y.H. | - |
dc.contributor.scopusid | 김현수(57191717719;57191718092) | - |
dc.date.modifydate | 20230620101535 | - |