Repeated Thermal Therapy Up-Regulates Endothelial Nitric Oxide Synthase and Augments Angiogenesis in a Mouse Model of Hindlimb Ischemia

• Akasaki Yuichi

  Department of Cardiovascular, Respiratory and Metabolic Medicine, Graduate School of Medicine, Kagoshima University

• Miyata Masaaki

  Department of Cardiovascular, Respiratory and Metabolic Medicine, Graduate School of Medicine, Kagoshima University

• Eto Hideyuki

  Department of Cardiovascular, Respiratory and Metabolic Medicine, Graduate School of Medicine, Kagoshima University

• Shirasawa Takahiro

  Department of Cardiovascular, Respiratory and Metabolic Medicine, Graduate School of Medicine, Kagoshima University

• Hamada Narisato

  Department of Cardiovascular, Respiratory and Metabolic Medicine, Graduate School of Medicine, Kagoshima University

• Ikeda Yoshiyuki

  Department of Cardiovascular, Respiratory and Metabolic Medicine, Graduate School of Medicine, Kagoshima University

• Biro Sadatoshi

  Department of Cardiovascular, Respiratory and Metabolic Medicine, Graduate School of Medicine, Kagoshima University

• Otsuji Yutaka

  Department of Cardiovascular, Respiratory and Metabolic Medicine, Graduate School of Medicine, Kagoshima University

• Tei Chuwa

  Department of Cardiovascular, Respiratory and Metabolic Medicine, Graduate School of Medicine, Kagoshima University

抄録

Background Nitric oxide (NO), constitutively produced by endothelial NO synthase (eNOS), plays roles in angiogenesis. Having reported that thermal therapy up-regulated the expression of arterial eNOS in hamsters, we investigated whether this therapy increased angiogenesis in mice with hindlimb ischemia. Methods and Results Unilateral hindlimb ischemia was induced in apolipoprotein E-deficient mice, which were divided into control and thermal therapy groups. The latter mice were placed in a far-infrared dry sauna at 41°C for 15 min and then at 34°C for 20 min once daily for 5 weeks. Laser Doppler perfusion imaging demonstrated that the ischemic limb/normal side blood perfusion ratio in the thermal therapy group was significantly increased beyond that in controls (0.79±0.04 vs 0.54±0.08, p<0.001). Significantly greater capillary density was seen in thermal therapy group (757±123 /mm² vs 416±20 /mm², p<0.01). Western blotting showed thermal therapy markedly increased hindlimb eNOS expression. To study possible involvement of eNOS in thermally induced angiogenesis, thermal therapy was given to mice with hindlimb ischemia with or without N^G-nitro-L-arginine methyl ester (L-NAME) administration for 5 weeks. L-NAME treatment eliminated angiogenesis induced using thermal therapy. Thermal therapy did not increase angiogenesis in eNOS-deficient mice. Conclusion Angiogenesis was induced via eNOS using thermal therapy in mice with hindlimb ischemia. (Circ J 2006; 70: 463 - 470)<br>

収録刊行物

• Circulation Journal

  Circulation Journal 70 (4), 463-470, 2006

  一般社団法人 日本循環器学会

キーワード

• Angiogenesis
• Nitric oxide synthase
• Thermal therapy

詳細情報

• CRID: 1390001205102610560
• NII論文ID: 110004497236
• NII書誌ID: AA11591968
• DOI: 10.1253/circj.70.463
• COI: 1:CAS:528:DC%2BD28XjvF2nu7g%3D
• ISSN: 13474820
• ISSN: 13469843
• ISSN: http://id.crossref.org/issn/13469843
• PubMed: 16565566
• Web Site: https://www.jstage.jst.go.jp/article/circj/70/4/70_4_463/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2007049610
• 本文言語コード: en
• データソース種別:
  • JaLC
  • Crossref
  • PubMed
  • CiNii Articles
• 抄録ライセンスフラグ: 使用不可