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Ischemia/reperfusion-induced death of cardiac myocytes: possible involvement of nitric oxide in the coordination of ATP supply and demand during ischemia.

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Title: Ischemia/reperfusion-induced death of cardiac myocytes: possible involvement of nitric oxide in the coordination of ATP supply and demand during ischemia.
Authors: Kawahara, Koichi Browse this author →KAKEN DB
Hachiro, Takeru Browse this author
Yokokawa, Takahiro Browse this author
Nakajima, Takayuki Browse this author
Yamauchi, Yoshiko Browse this author
Nakayama, Yukako Browse this author
Keywords: Ischemia
Reperfusion
Cultured cardiac myocytes
Nitric oxide
ATP
Lactate
Issue Date: Jan-2006
Publisher: Elsevier Ltd
Journal Title: Journal of Molecular and Cellular Cardiology
Volume: 40
Issue: 1
Start Page: 35
End Page: 46
Publisher DOI: 10.1016/j.yjmcc.2005.06.020
PMID: 16324709
Abstract: Nitric oxide (NO) has been known to play various functional and pathological roles as an intracellular or intercellular messenger in the heart. In this study, we investigated whether NO produced during ischemia was involved in the coordination of ATP supply and demand, and also in protection from cell death using cultured cardiac myocytes. Unexpectedly, the survival rate of myocytes for 3 h simulated ischemia (SI) was increased as compared with that for 2 h SI at 24 h after reperfusion. The cellular ATP level at 3 h after the start of SI was increased compared with that at 2 h, and was almost the same as that before the start of SI. The cellular ATP level at 3 h SI was significantly reduced by either the inhibition of nitric oxide synthase (NOS) or scavenging of NO. Either the inhibition of NOS or the scavenging of NO during SI for 3 h also resulted in a significant decrease in the survival rate of myocytes. Immunocytochemical and Western blot analyses revealed that the expression of nNOS was most evident in cardiac myocytes, but no significant change was observed in the expression of all three NOS isoforms at 2 h SI and at 3 h SI. The fluorescent intensity of DAF-FM was significantly increased at 3 h SI as compared with that at 2 h SI, and the increase in DAF fluorescence during SI was almost completely suppressed by treatment with vinyl-l-NIO (l-VNIO), a potent specific inhibitor of nNOS. In addition, treatment with l-VNIO decreased the cellular ATP level and survival rate. This study suggested that the enhanced production of NO was critical in balancing ATP supply and demand during ischemia, and also in protecting cells from ischemia/reperfusion injury.
Relation: http://www.sciencedirect.com/science/journal/00222828
Type: article (author version)
URI: http://hdl.handle.net/2115/14611
Appears in Collections:情報科学院・情報科学研究院 (Graduate School of Information Science and Technology / Faculty of Information Science and Technology) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 河原 剛一

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