L-Arginine protects human heart cells from low-volume anoxia and reoxygenation

Division of Cardiac Surgery, University of Toronto, Toronto, Ontario, M5G 2C4 Canada Protective effects of L -arginine were evaluated in a human ventricular heart cell model of low-volume anoxia and reoxygenation independent of alternate cell types. Cell cultures were subjected to 90 min of low-volu...

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Published in:American journal of physiology. Heart and circulatory physiology 2002-03, Vol.282 (3), p.H805-H815
Main Authors: Shiono, Noritsugu, Rao, Vivek, Weisel, Richard D, Kawasaki, Muneyasu, Li, Ren-Ke, Mickle, Donald A. G, Fedak, Paul W. M, Tumiati, Laura C, Ko, Lawrence, Verma, Subodh
Format: Article
Language:English
Subjects:
Arginine - pharmacology
Cell Hypoxia - drug effects
Cells, Cultured
Heart - drug effects
Heart - physiology
Humans
Immunohistochemistry
Models, Cardiovascular
Myocardium - cytology
Myocardium - enzymology
Nitric Oxide Synthase - metabolism
Nitric Oxide Synthase Type II
Nitric Oxide Synthase Type III
Oxidation-Reduction
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Summary:Division of Cardiac Surgery, University of Toronto, Toronto, Ontario, M5G 2C4 Canada Protective effects of L -arginine were evaluated in a human ventricular heart cell model of low-volume anoxia and reoxygenation independent of alternate cell types. Cell cultures were subjected to 90 min of low-volume anoxia and 30 min of reoxygenation. L -Arginine (0-5.0 mM) was administered during the preanoxic period or the reoxygenation phase. Nitric oxide (NO) production, NO synthase (NOS) activity, cGMP levels, and cellular injury were assessed. To evaluate the effects of the L -arginine on cell signaling, the effects of the NOS antagonist N G -nitro- L -arginine methyl ester, NO donor S -nitroso- N -acetyl-penicillamine, guanylate cyclase inhibitor methylene blue, cGMP analog 8-bromo-cGMP, and ATP-sensitive K + channel antagonist glibenclamide were examined. Our data indicate that low-volume anoxia and reoxygenation increased NOS activity and facilitated the conversion of L -arginine to NO, which provided protection against cellular injury in a dose-dependent fashion. In addition, L -arginine cardioprotection was achieved by the activation of guanylate cyclase, leading to increased cGMP levels in human heart cells. This action involves a glibenclamide-sensitive, NO-cGMP-dependent pathway. ventricular myocytes; cardiac surgery; nitric oxide
ISSN:0363-6135
1522-1539
DOI:10.1152/ajpheart.00594.2001