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- ISHIOKA Haruhiko
- <I>Third Department of Internal Medicine, Showa University School of Medicine</I>
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- GESHI Eiichi
- <I>Third Department of Internal Medicine, Showa University School of Medicine</I>
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- ARATA Hirohisa
- <I>Third Department of Internal Medicine, Showa University School of Medicine</I>
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- KATAGIRI Takashi
- <I>Third Department of Internal Medicine, Showa University School of Medicine</I>
抄録
We studied the mechanism of the preconditioning (PC) on ischemic cellular injury based on the specific biochemical characteristics of the sarcoplasmic reticulum (SR) and mitochondria (Mt) . Forty dogs were divided into two groups: 1) PC group (four times of LAD occlusion for 5 min with each 10 min interval), 2) I group (no preconditioning) . Then 60 min ischemia and reperfusion with continuous on-line recordings of hemodynamics and % segment shortening (SS) were performed. Myocardial ischemic injury was quantitated by the biochemical analyses of SR and Mt. After 60 min reflow, % SS of the ischemic portion was reduced to -32.5 ± 18.6% of the previous control level in the I group. In the PC group this was kept at -16.3±11.9% of control. Ca++-ATPase activity of the SR showed a significantly higher value in the PC group (11.1 ± 1.1 μmoles Pi/mg protein/hr) than in the I group (9.5±1.9) . Also on SDS gel electrophoresis of SR, major ATPase protein was well maintained in the PC group. Both respiratory and dinitrophenol-ATPase activities of mitochondria were also higher in the PC group than in the I group. Ischemic preconditioning inhibited degradations of membranous microorgans and maintained contractile function in the ischemic myocardium.
収録刊行物
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- The Showa University Journal of Medical Sciences
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The Showa University Journal of Medical Sciences 7 (1), 71-82, 1995
昭和大学学士会
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詳細情報 詳細情報について
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- CRID
- 1390282679350729344
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- NII論文ID
- 130004190291
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- ISSN
- 21850968
- 09156380
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- Crossref
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可