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Hyperglycemia attenuates myocardial preconditioning of remifentanil

Authors
 Hyun Soo Kim  ;  So Yeon Kim  ;  Young Lan Kwak  ;  Ki Chul Hwang  ;  Yon Hee Shim 
Citation
 JOURNAL OF SURGICAL RESEARCH, Vol.174(2) : 231-237, 2012 
Journal Title
 JOURNAL OF SURGICAL RESEARCH 
ISSN
 0022-4804 
Issue Date
2012
MeSH
Analgesics, Opioid/pharmacology ; Analgesics, Opioid/therapeutic use* ; Animals ; Animals, Newborn ; Apoptosis/drug effects ; Calcium/metabolism ; Cell Survival/drug effects ; Cells, Cultured ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Hyperglycemia/complications* ; Hyperglycemia/metabolism ; Hypoxia/complications* ; Hypoxia/drug therapy ; Hypoxia/metabolism ; Ischemic Preconditioning, Myocardial/methods* ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/metabolism ; Piperidines/pharmacology ; Piperidines/therapeutic use* ; Proto-Oncogene Proteins c-akt/metabolism ; Rats ; Rats, Sprague-Dawley
Keywords
hyperglycemia ; hypoxia-reoxygenation injury ; remifentanil ; myocardial preconditioning
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.
Full Text
http://www.sciencedirect.com/science/article/pii/S0022480411000552
DOI
21392805
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Anesthesiology and Pain Medicine (마취통증의학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
Yonsei Authors
Kwak, Young Lan(곽영란) ORCID logo https://orcid.org/0000-0002-2984-9927
Kim, So Yeon(김소연) ORCID logo https://orcid.org/0000-0001-5352-157X
Shim, Yon Hee(심연희) ORCID logo https://orcid.org/0000-0003-1921-3391
Hwang, Ki Chul(황기철)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/91109
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