title: Effect of Waon therapy on oxidative stress in chronic heart failure.
abstract: BACKGROUND
  A previous report by our team showed that Waon therapy, using a far infrared-ray dry sauna at 60°C, improves cardiac and vascular function in patients with chronic heart failure (CHF). The purpose of the present study was to clarify the effect of Waon therapy on oxidative stress in CHF patients and investigate its mechanism by animal experiments.
  
  
  RESULTS
  Forty patients with CHF were divided into control (n=20) and Waon therapy (n=20) groups. All patients received standard optimal medications for CHF. Waon therapy group was treated with Waon therapy daily for 4 weeks. After 4 weeks of Waon therapy, concentrations of hydroperoxide and brain natriuretic peptide (BNP) decreased significantly (hydroperoxide, 422±116 to 327±88U.CARR, P<0.001; BNP, 402±221 to 225±137pg/ml, P<0.001), and the nitric oxide metabolites increased (71.2±35.4 to 92.0±40.5mmol/L, P<0.05). In contrast, none of these variables changed over the 4-week interval in the control group. Furthermore, animal experiments were performed using TO-2 cardiomyopathic hamsters. On immunohistochemistry, cardiac expression of 4-hydroxy-2-nonenal, a marker of oxidative stress, was decreased in the 4-week Waon therapy compared to untreated hamsters. On Western blotting, cardiac expressions of heat shock protein (HSP) 27, manganese superoxide dismutase and HSP32, which reduce oxidative stress, were significantly upregulated in the 4-week Waon therapy compared to untreated hamsters.
  
  
  CONCLUSIONS
  Waon therapy decreases oxidative stress in patients and hamsters with heart failure.
authors.affiliation: Department of Cardiovascular, Respiratory and Metabolic Medicine, Graduate School of Medicine, Kagoshima University, Kagoshima, Japan.
authors.forename: Shoji
authors.initials: S
authors.lastname: Fujita
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Ikeda
authors.forename: Masaaki
authors.initials: M
authors.lastname: Miyata
authors.forename: Takuro
authors.initials: T
authors.lastname: Shinsato
authors.forename: Takuro
authors.initials: T
authors.lastname: Kubozono
authors.forename: So
authors.initials: S
authors.lastname: Kuwahata
authors.forename: Narisato
authors.initials: N
authors.lastname: Hamada
authors.forename: Takahiro
authors.initials: T
authors.lastname: Miyauchi
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Yamaguchi
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Torii
authors.forename: Shuichi
authors.initials: S
authors.lastname: Hamasaki
authors.forename: Chuwa
authors.initials: C
authors.lastname: Tei
mesh_terms: D000368:Aged; D000447:Aldehydes / Q000097:blood; D000818:Animals; D015415:Biomarkers; D002311:Cardiomyopathy, Dilated / Q000097:blood / Q000235:genetics; D002317:Cardiovascular Agents / Q000627:therapeutic use; D003131:Combined Modality Therapy; D006224:Cricetinae; D004195:Disease Models, Animal; D005260:Female; D005786:Gene Expression Regulation; D006333:Heart Failure / Q000188:drug therapy / Q000378:metabolism / Q000628:therapy*; D006360:Heat-Shock Proteins / Q000097:blood / Q000235:genetics; D006358:Hot Temperature / Q000627:therapeutic use*; D006801:Humans; D006861:Hydrogen Peroxide / Q000097:blood; D007259:Infrared Rays / Q000627:therapeutic use*; D008297:Male; D008647:Mesocricetus; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood; D009569:Nitric Oxide / Q000097:blood; D018384:Oxidative Stress; D013482:Superoxide Dismutase / Q000097:blood / Q000235:genetics
chemical_list: D000447:Aldehydes; D015415:Biomarkers; D002317:Cardiovascular Agents; D006360:Heat-Shock Proteins; D020097:Natriuretic Peptide, Brain; D009569:Nitric Oxide; D006861:Hydrogen Peroxide; D013482:Superoxide Dismutase; C027576:4-hydroxy-2-nonenal