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Cardioprotection via modulation of calcium homeostasis by thiopental in hypoxia-reoxygenated neonatal rat cardiomyocytes

Authors
 Hyun-Soo Kim  ;  Ki-Chul Hwang  ;  Wyun-Kon Park 
Citation
 YONSEI MEDICAL JOURNAL, Vol.51(2) : 187-196, 2010 
Journal Title
 YONSEI MEDICAL JOURNAL 
ISSN
 0513-5796 
Issue Date
2010
MeSH
Animals ; Apoptosis ; Calcium/metabolism* ; Cell Hypoxia/physiology* ; Cell Survival/drug effects ; Cells, Cultured ; GABA Modulators/pharmacology* ; Homeostasis/drug effects ; Immunoblotting ; In Situ Nick-End Labeling ; Membrane Potential, Mitochondrial/drug effects ; Microscopy, Confocal ; Myocytes, Cardiac/drug effects* ; Myocytes, Cardiac/metabolism* ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction ; Thiopental/pharmacology*
Keywords
Ca2+ homeostasis ; Thiopental ; cardiomyocytes ; hypoxia-reoxygenation
Abstract
PURPOSE: Ca(2+) homeostasis plays an important role in myocardial cell injury induced by hypoxia-reoxygenation, and prevention of intracellular Ca(2+) overload is key to cardioprotection. Even though thiopental is a frequently used anesthetic agent, little is known about its cardioprotective effects, particularly in association with Ca(2+) homeostasis. We investigated whether thiopental protects cardiomyocytes against hypoxia-reoxygenation injury by regulating Ca(2+) homeostasis. MATERIALS AND METHODS: Neonatal rat cardiomyocytes were isolated. Cardiomyocytes were exposed to different concentrations of thiopental and immediately replaced in the hypoxic chamber to maintain hypoxia. After 1 hour of exposure, a culture dish was transferred to the CO(2) incubator and cells were incubated at 37 for 5 hours. At the end of the experiments, the authors assessed cell protection using immunoblot analysis and caspase activity. The mRNA of genes involved in Ca(2+) homeostasis, mitochondrial membrane potential, and cellular Ca(2+) levels were examined. RESULTS: In thiopental-treated cardiomyocytes, there was a decrease in expression of the proapoptotic protein Bax, caspase-3 activation, and intracellular Ca(2+) content. In addition, both enhancement of anti-apoptotic protein Bcl-2 and activation of Erk concerned with survival were shown. Furthermore, thiopental attenuated alterations of genes involving Ca(2+) regulation and significantly modulated abnormal changes of NCX and SERCA2a genes in hypoxia-reoxygenated neonatal cardiomyocytes. Thiopental suppressed disruption of mitochondrial membrane potential (DeltaPsi(m)) induced by hypoxia-reoxygenation. CONCLUSION: Thiopental is likely to modulate expression of genes that regulate Ca(2+) homeostasis, which reduces apoptotic cell death and results in cardioprotection
Files in This Item:
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DOI
10.3349/ymj.2010.51.2.187
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
Park, Wyun Kon(박윤곤)
Hwang, Ki Chul(황기철)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/100612
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