title: Prevention of arterial stiffening by using low-dose atorvastatin in diabetes is associated with decreased malondialdehyde.
abstract: BACKGROUND
  Without affecting the lipid profile, a low-dose treatment with atorvastatin contributes to the reduction of oxidative stress, inflammation, and adverse cardiovascular events in diabetes. In this study, we investigated whether low-dose atorvastatin exerts any beneficial effect on vascular dynamics in streptozotocin (STZ)-induced diabetes in male Wistar rats.
  
  
  METHODS
  Diabetes was induced using a single tail-vein injection of STZ at 55 mg kg-1. The diabetic rats were treated daily with atorvastatin (10 mg kg-1 by oral gavage) for 6 weeks. They were also compared with untreated age-matched diabetic controls. Arterial wave reflection was derived using the impulse response function of the filtered aortic input impedance spectra. A thiobarbituric acid reactive substances measurement was used to estimate the malondialdehyde content.
  
  
  RESULTS
  The high plasma level of total cholesterol in the diabetic rats did not change in response to this low-dose treatment with atorvastatin. Atorvastatin resulted in a significant increase of 15.4% in wave transit time and a decrease of 33.5% in wave reflection factor, suggesting that atorvastatin may attenuate the diabetes-induced deterioration in systolic loads imposed on the heart. This was in parallel with its lowering of malondialdehyde content in plasma and aortic walls in diabetes. Atorvastatin therapy also prevented the diabetes-related cardiac hypertrophy, as evidenced by the diminished ratio of left ventricular weight to body weight.
  
  
  CONCLUSIONS
  These findings indicate that low-dose atorvastatin might protect diabetic vasculature against diabetes-associated deterioration in aorta stiffness and cardiac hypertrophy, possibly through its decrease of lipid oxidation-derived malondialdehyde.
authors.affiliation: Department of Surgery, National Taiwan University Hospital, Taipei, Taiwan; Department of Surgery, National Taiwan University Hospital, Hsin-Chu Branch, Hsin-Chu, Taiwan; Department of Physiology, College of Medicine, National Taiwan University, Taipei, Taiwan.
authors.forename: Chih-Hsien
authors.initials: CH
authors.lastname: Wang
authors.affiliation: Department of Surgery and Traumatology, National Taiwan University Hospital, Taipei, Taiwan.
authors.forename: Ru-Wen
authors.initials: RW
authors.lastname: Chang
authors.affiliation: Department of Physiology, College of Medicine, National Taiwan University, Taipei, Taiwan.
authors.forename: Ya-Hui
authors.initials: YH
authors.lastname: Ko
authors.affiliation: Department of Surgery and Traumatology, National Taiwan University Hospital, Taipei, Taiwan.
authors.forename: Pi-Ru
authors.initials: PR
authors.lastname: Tsai
authors.affiliation: Department of Surgery, National Taiwan University Hospital, Taipei, Taiwan.
authors.forename: Shoei-Shen
authors.initials: SS
authors.lastname: Wang
authors.affiliation: Department of Surgery, National Taiwan University Hospital, Taipei, Taiwan.
authors.forename: Yih-Sharng
authors.initials: YS
authors.lastname: Chen
authors.affiliation: Department of Surgery and Traumatology, National Taiwan University Hospital, Taipei, Taiwan.
authors.forename: Wen-Je
authors.initials: WJ
authors.lastname: Ko
authors.affiliation: Department of Emergency Medicine, National Taiwan University Hospital, Taipei, Taiwan.
authors.forename: Chun-Yi
authors.initials: CY
authors.lastname: Chang
authors.affiliation: Institute of Biomedical Engineering, College of Medicine and Engineering, National Taiwan University, Taipei, Taiwan.
authors.forename: Tai-Horng
authors.initials: TH
authors.lastname: Young
authors.affiliation: Department of Physiology, College of Medicine, National Taiwan University, Taipei, Taiwan.
authors.forename: Kuo-Chu
authors.initials: KC
authors.lastname: Chang
mesh_terms: D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000378:metabolism; D000069059:Atorvastatin; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D002097:C-Reactive Protein / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000378:metabolism* / Q000503:physiopathology*; D004305:Dose-Response Relationship, Drug; D005227:Fatty Acids / Q000097:blood; D017127:Glycation End Products, Advanced / Q000378:metabolism; D006439:Hemodynamics / Q000187:drug effects; D006538:Heptanoic Acids / Q000008:administration & dosage* / Q000494:pharmacology*; D008239:Lysine / Q000031:analogs & derivatives / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000097:blood / Q000378:metabolism*; D009929:Organ Size / Q000187:drug effects; D011758:Pyrroles / Q000008:administration & dosage* / Q000494:pharmacology*; D017208:Rats, Wistar; D013311:Streptozocin; D059289:Vascular Stiffness / Q000187:drug effects*
chemical_list: D001786:Blood Glucose; D005227:Fatty Acids; D017127:Glycation End Products, Advanced; D006538:Heptanoic Acids; D011758:Pyrroles; D008315:Malondialdehyde; D013311:Streptozocin; D002097:C-Reactive Protein; D001120:Arginine; D002784:Cholesterol; D000069059:Atorvastatin; C062187:pentosidine; D008239:Lysine