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Hyperglycemia attenuates myocardial preconditioning of remifentanil

Title
Hyperglycemia attenuates myocardial preconditioning of remifentanil
Authors
Kim H.S.Kim S.Y.Kwak Y.L.Hwang K.C.Shim Y.H.
Ewha Authors
김현수
Issue Date
2012
Journal Title
Journal of Surgical Research
ISSN
0022-4804JCR Link
Citation
vol. 174, no. 2, pp. 231 - 237
Indexed
SCI; SCIE; SCOPUS WOS scopus
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.
DOI
10.1016/j.jss.2011.01.018
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자연과학대학 > 생명과학전공 > Journal papers
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