Enhanced generation of reactive oxygen species in the limb skeletal muscles from a murine infarct model of heart failure

Hiroyuki Tsutsui, Tomomi Ide, Shunji Hayashidani, Nobuhiro Suematsu, Tetsuya Shiomi, Jing Wen, Kei Ichiro Nakamura, Kazuhiro Ichikawa, Hideo Utsumi, Akira Takeshita

研究成果: Contribution to journalArticle査読

110 被引用数 (Scopus)

抄録

Background - The generation of reactive oxygen species (ROS) is enhanced in the failing myocardium. We hypothesized that ROS were also increased in the limb skeletal muscles in heart failure. Methods and Results - Myocardial infarction (MI) was created in mice by ligating the left coronary artery. After 4 weeks, the left ventricle was dilated and contractility was diminished by echocardiography. Left ventricular end-diastolic pressure was elevated after MI in association with an increase in lung weight/body weight and the presence of pleural effusion. The generation of ROS in the limb muscles, including the soleus and gastrocnemius muscles, which were excised after MI, was measured by electron spin resonance spectroscopy with 4-hydroxy-2,2,6,6-tetramethyl-piperidine-N-oxyl (hydroxy-TEMPO). Overall, generation was increased, but it was attenuated in the presence of dimethylthiourea or 4,5-dihydroxy-1,2-benzenedisulfonic disodium salt in the reaction mixture, indicating increased generation of hydroxyl radicals originating from superoxide anion. Thiobarbituric acid-reactive substance formation was also increased in muscles after MI. Mitochondrial complex I and III activities were both decreased after MI, which may have caused the functional uncoupling of the respiratory chain and ROS production. Antioxidant enzyme activities, including superoxide dismutase, catalase, and glutathione peroxidase, were comparable between groups. Conclusions - Skeletal muscle in post-MI heart failure expressed an increased amount of ROS in association with ROS-mediated lipid peroxidation. This supports the hypothesis that oxidative stress may cause (at least in part) skeletal muscle dysfunction in heart failure.

本文言語英語
ページ(範囲)134-136
ページ数3
ジャーナルCirculation
104
2
DOI
出版ステータス出版済み - 7 10 2001

All Science Journal Classification (ASJC) codes

  • 循環器および心血管医学
  • 生理学(医学)

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