城西大学機関リポジトリJURAAcute lethal crush-injured rats can be successfully rescued by a single injection of high-dose dexamethasone through a pathway involving PI3K-Akt-eNOS signaling

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Acute lethal crush-injured rats can be successfully rescued by a single injection of high-dose dexamethasone through a pathway involving PI3K-Akt-eNOS signaling

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ID	JOS-TA.0b013e3182905f11
著者：名前	村田, 勇/大井, 一弥/庄司, 真悟/本橋, 洋平/姜, 美和/大竹, 一男/木村, 聡一郎/上田, 秀雄/中野, 玄也/薗田, 邦博/井上, 裕/内田, 博之/金本, 郁男/森本, 雍憲/小林, 順
著者：別形式	Murata, Isamu / Ooi, Kazuya / Shoji, Shingo / Motohashi, Yohei / Kan, Miwa / Ohtake, Kazuo / Kimura, Soichiro / Ueda, Hideo / Nakano, Genya / Sonoda, Kunihiro / Inoue, Yutaka / Uchida, Hiroyuki / Kanamoto, Ikuo / Morimoto, Yasunori / Kobayashi, Jun
著者：カナ	ムラタ, イサム/オオイ, カズヤ/ショウジ, シンゴ/モトハシ, ヨウヘイ/カン, ミワ/オオタケ, カズオ/キムラ, ソウイチロウ/ウエダ, ヒデオ/ナカノ, ゲンヤ/ソノダ, クニヒロ/イノウエ, ユタカ/ウチダ, ヒロユキ/カナモト, イクオ/モリモト, ヤスノリ/コバヤシ, ジュン
著者：所属	城西大学薬学部医薬品安全性学講座 / 鈴鹿医療科学大学薬学部 / 城西大学薬学部病院薬剤学講座 / 城西大学薬学部病院薬剤学講座 / 城西大学薬学部医薬品安全性学講座 / 城西大学薬学部医療栄養学科病態解析学講座 / 城西大学薬学部病院薬剤学講座 / 城西大学薬学部病院薬剤学講座 / 城西大学薬学部医療栄養学科病態解析学講座 / 金城学院大学生活環境学部食環境栄養学科 / 城西大学薬学部医薬品安全性学講座 / 城西大学薬学部医療栄養学科病態解析学講座 / 城西大学薬学部医薬品安全性学講座 / 城西大学薬学部病院薬剤学講座 /城西大学薬学部医療栄養学科病態解析学講座
著者：所属(別形式）	Josai University, Faculty of Pharmaceutical Science, Laboratory of Drug Safety Management / Suzuka University of Medical Science, Faculty of Pharmaceutical Science, Department of Clinical Pharmacology / Josai University, Faculty of Pharmaceutical Science, Laboratory of Hospital Pharmacy / Josai University, Faculty of Pharmaceutical Science, Laboratory of Hospital Pharmacy / Josai University, Faculty of Pharmaceutical Science, Laboratory of Drug Safety Management / Josai University, Faculty of Pharmaceutical Science, Department of Clinical Dietetics and Human Nutrition, Division of Pathophysiology / Kinjo Gakuin University, College of Human Life and Environment, Department of Food and Nutritional Environment / Josai University, Faculty of Pharmaceutical Science, Laboratory of Drug Safety Management / Josai University, Faculty of Pharmaceutical Science, Department of Clinical Dietetics and Human Nutrition, Division of Pathophysiology / Josai University, Faculty of Pharmaceutical Science, Laboratory of Drug Safety Management / Josai University, Faculty of Pharmaceutical Science, Laboratory of Hospital Pharmacy / Josai University, Faculty of Pharmaceutical Science, Department of Clinical Dietetics and Human Nutrition, Division of Pathophysiology
著者版フラグ	author
出版者	Lippincott Williams & Wilkins
NCID	AA12565125
冊子ISSN	21630755
電子ISSN	21630763
掲載誌名	Journal of Trauma and Acute Care Surgery
巻	75
号	2
刊行年月	2013-08
開始ページ	214
終了ページ	249
コンテンツ作成日	2013-01-31
コンテンツ修正日	2013-02-25
コンテンツ登録日	2015-02-06
識別番号：DOI	info:doi/10.1097/TA.0b013e3182905f11
識別番号：DOI（リンク）	http://dx.doi.org/10.1097/TA.0b013e3182905f11
抄録	Crush syndrome (CS) is characterized by ischemia/reperfusion (I/R)-induced rhabdomyolysis and the subsequent onset of systemic inflammation. CS is associated with a high mortality, even when patients are treated with conventional therapy. We hypothesized treatment of lethal CS rat model with dexamethasone (DEX) have therapeutic effects on the laboratory findings and clinical course and outcome. Methods: To create a CS model, anesthetized rats were subjected to bilateral hind limb compression with rubber tourniquets for 5 hours, and randomly divided into 3 groups: saline-treated CS, and low (0.1 mg/kg) and high doses (5.0 mg/kg) of DEX-treated CS groups. Saline for the CS group or DEX for the DEX-treated CS groups was intravenously administered immediately before reperfusion. Under continuous monitoring and recording of arterial blood pressures, blood and tissue samples were collected for histological and biochemical analysis at designated time period before and after reperfusion. Results: Under continuous monitoring and recording of arterial blood pressures, blood and tissue samples were collected for histological and biochemical analysis at designated time period before and after reperfusion. Ischemic compression of rat hind limbs reduced the nitrite content in the crushed muscle, and the subsequent reperfusion induced reactive oxygen species-mediated circulatory collapse and systemic inflammation, finally resulting in a mortality rate of 76% by 48 hours after reperfusion. A single injection of high-dose DEX *Abstract immediately before reperfusion activated endothelial nitric oxide synthase (eNOS) by sequential phosphorylation through the non-genomic phosphoinositide 3-kinase (PI3K)-Akt-eNOS signaling pathway. DEX also exhibited anti-inflammatory effects by modulating pro- and anti-inflammatory mediators, consequently suppressing myeloperoxidase activities and subsequent systemic inflammation, showing a complete recovery of the rats from lethal CS. Conclusion: These results indicate that high-dose DEX reduces systemic inflammation and contributes to the improved survival rate in a rat CS model.
キーワード	crush syndrome/ischemia/reperfusion/nitric oxide/Dexamethasone/nitrite
言語	eng
資源タイプ	text
ジャンル	01学術雑誌論文 / Journal Article
フォーマット	application/pdf
権利	Publisher's edition: c2013 Lippincott Williams & Wilkins, Inc.
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このアイテムを表示する：URI	http://libir.josai.ac.jp/il/meta_pub/G0000284repository_JOS-TA.0b013e3182905f11

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