Generation of Free Radicals and the Damage Done to the Sarcoplasmic Reticulum During Reperfusion Injury Following Brief Ischemia in the Canine Heart

• ITOH Seiji

  The Third Department of Internal Medicine, School of Medicine, Showa University

• YANAGISHITA Toshikuni

  The Third Department of Internal Medicine, School of Medicine, Showa University

• AOKI Shuichi

  The Third Department of Internal Medicine, School of Medicine, Showa University

• KOBA Shinji

  The Third Department of Internal Medicine, School of Medicine, Showa University

• IWATA Toshiki

  The Third Department of Internal Medicine, School of Medicine, Showa University

• ISHIOKA Haruhiko

  The Third Department of Internal Medicine, School of Medicine, Showa University

• ARATA Hirohisa

  The Third Department of Internal Medicine, School of Medicine, Showa University

• MUKAE Shuji

  The Third Department of Internal Medicine, School of Medicine, Showa University

• GESHI Eiichi

  The Third Department of Internal Medicine, School of Medicine, Showa University

• KONNO Noburu

  The Third Department of Internal Medicine, School of Medicine, Showa University

• KATAGIRI Takashi

  The Third Department of Internal Medicine, School of Medicine, Showa University

• UTSUMI Hideo

  Department of Physical chemistry, Faculty of Pharmaceutical Sciences, Kyushu University

抄録

Free radical generation was studied by the electron spin resonance (ESR) technique using α-phenyl N tert butyl nitrone (PBN) in a brief ischemia-reperfusion model of the canine heart, and correlated with biochemical changes of the sarcoplasmic reticulum (SR). ESR spectra (aH=0.3-0.4mT, aN=1.43-1.58mT) were observed as PBN spin adducts, which peaked at levels 5-fold above the control levels at 5 min after reperfusion. The simulated coupling constants of PBN spin adducts suggested that the sample should contain at least 2 carbon-centered radicals at 5 min after reperfusion (radical A: aH=0.350mT, aN=1.485mT; radical B: aH=0.370mT, aN=1.615mT). At this time point, a significant reduction in Ca-ATPase activity of the SR was found without degradation of the major ATPase protein. Superoxide dismutase (SOD) significantly reduced the intensity of the PBN spin adduct signals and preserved the Ca-ATPase activity of the SR to 80% of the control level. Reperfusion injury after brief ischemia may be the result of inactivation of intracellular Ca-ATPase by free radicals generated during reperfusion, and SOD contributes to the protective effect by scavenging the radicals.

収録刊行物

• Japanese circulation journal

  Japanese circulation journal 63 (5), 373-378, 1999-04-20

  社団法人日本循環器学会

キーワード

• Canine heart
• Electron spin responance
• Reperfusion injury
• Sarcoplasmic reticulum
• Superoxide dismutase

詳細情報

• CRID: 1570009752159579264
• NII論文ID: 110002608500
• NII書誌ID: AA00690731
• ISSN: 00471828
• Web Site: https://search.jamas.or.jp/link/ui/1999214431
• 本文言語コード: en
• データソース種別:
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