title: Time-dependent changes of myocardial and systemic oxidative stress are dissociated after myocardial infarction.
abstract: Reactive oxygen species (ROS) is increased in myocardium after myocardial infarction (MI), which may play a causal role in cardiac remodelling. However, there is scant direct and longitudinal evidence that systemic oxidative stress is enhanced accompanying an increase of ROS in myocardium. The authors conducted a comprehensive investigation of ROS markers by simultaneously sampling urine, blood and myocardium and in vivo ESR for the heart at different stages of post-MI cardiac remodelling in mouse with permanent occlusion of left coronary artery. Systemic oxidative markers increased at early days after MI and were normalized later. In contrast, TBARS and 4-hexanoyl-Lys staining were increased in non-infarct myocardium at day 28. The enhancement of ESR signal decay of methoxycarbonyl-PROXYL measured at the chest was associated with the progression of left ventricle dilatation and dysfunction. This study provided the direct evidence that redox alteration and production of ROS occurred in myocardium during the progression of cardiac remodelling and failure; however, ROS marker levels in blood and urine do not reflect the production of ROS from failing myocardium.
authors.affiliation: Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
authors.forename: Takahiro
authors.initials: T
authors.lastname: Inoue
authors.forename: Tomomi
authors.initials: T
authors.lastname: Ide
authors.forename: Mayumi
authors.initials: M
authors.lastname: Yamato
authors.forename: Masayoshi
authors.initials: M
authors.lastname: Yoshida
authors.forename: Takaki
authors.initials: T
authors.lastname: Tsutsumi
authors.forename: Makoto
authors.initials: M
authors.lastname: Andou
authors.forename: Hideo
authors.initials: H
authors.lastname: Utsumi
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Tsutsui
authors.forename: Kenji
authors.initials: K
authors.lastname: Sunagawa
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000818:Animals; D000975:Antioxidants / Q000032:analysis; D015415:Biomarkers / Q000032:analysis; D054059:Coronary Occlusion / Q000150:complications; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000032:analysis / Q000652:urine; D018450:Disease Progression; D004578:Electron Spin Resonance Spectroscopy; D007150:Immunohistochemistry; D008297:Male; D051379:Mice; D009203:Myocardial Infarction / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D018384:Oxidative Stress / Q000502:physiology*; D017382:Reactive Oxygen Species / Q000032:analysis*; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D013995:Time
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D017382:Reactive Oxygen Species; D017392:Thiobarbituric Acid Reactive Substances; D000080242:8-Hydroxy-2'-Deoxyguanosine; D003849:Deoxyguanosine