title: [Effects of atorvastatin, fluvastatin, pravastatin, and simvastatin on endothelial function, lipid peroxidation, and aortic atherosclerosis in hypercholesterolemic rabbits].
abstract: OBJECTIVE
  To compare the effects of atorvastatin, fluvastatin, pravastatin, and simvastatin on endothelial function, aortic atherosclerosis, and the content of malondialdehyde (MDA) in native and oxidized LDL and in the arterial wall of hypercholesterolemic rabbits after adjusting the dosages of those statins to reduce total serum cholesterol levels to similar values.
  
  
  METHODS
  Male rabbits were divided into the following 6 groups of 10 animals (n=10): 1) GH (control)--hypercholesterolemic animals; 2) GA--atorvastatin; 3) GF--fluvastatin; 4) GP--pravastatin; 5) GS--simvastatin; and 6) GN--normal. The animals were fed a standard food preparation enriched with 0.5% cholesterol and 2% coconut oil for 45 days. Fifteen days after beginning the experiment, atorvastatin, fluvastatin, pravastatin and simvastatin were administered for 15 days through gavage, and the dosages were adjusted to obtain similar cholesterol values in each group. At the end of the experiment, a blood sample was withdrawn for determining total cholesterol and separating the lipoproteins, and a segment of the thoracic aorta was removed to be used for studying endothelial function and lipid peroxidation, and for measuring aortic atherosclerosis in histological sections.
  
  
  RESULTS
  The statins significantly reduced total serum cholesterol levels, LDL-cholesterol levels, and aortic atherosclerosis. The MDA content was also significantly reduced in native and oxidized LDL, as well as in the arterial wall. Endothelium-dependent relaxation was significantly greater in the treated group compared with that in the hypercholesterolemic group.
  
  
  CONCLUSIONS
  The statins, at dosages adjusted, had a significant and similar effect in reducing lipid peroxidation in native and oxidized LDL-C and in arterial walls, in decreasing aortic atherosclerosis, and in reverting endothelial dysfunction.
authors.affiliation: Faculdade de Ciências Médicas, Unicamp, Campinas, SP. parjorge@terra.com.br
authors.forename: Paulo Afonso Ribeiro
authors.initials: PA
authors.lastname: Jorge
authors.forename: Eros Antonio de
authors.initials: EA
authors.lastname: Almeida
authors.forename: Michiko R
authors.initials: MR
authors.lastname: Ozaki
authors.forename: Mariana
authors.initials: M
authors.lastname: Jorge
authors.forename: Adriano
authors.initials: A
authors.lastname: Carneiro
mesh_terms: D000818:Animals; D000924:Anticholesteremic Agents / Q000494:pharmacology*; D001018:Aortic Diseases / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D001161:Arteriosclerosis / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D000069059:Atorvastatin; D002784:Cholesterol / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood / Q000187:drug effects; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D005229:Fatty Acids, Monounsaturated / Q000494:pharmacology; D000077340:Fluvastatin; D006538:Heptanoic Acids / Q000494:pharmacology; D006937:Hypercholesterolemia / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D007211:Indoles / Q000494:pharmacology; D015227:Lipid Peroxidation / Q000187:drug effects*; D008297:Male; D008315:Malondialdehyde / Q000032:analysis; D017035:Pravastatin / Q000494:pharmacology; D011758:Pyrroles / Q000494:pharmacology; D011817:Rabbits; D019821:Simvastatin / Q000494:pharmacology
chemical_list: D000924:Anticholesteremic Agents; D008078:Cholesterol, LDL; D005229:Fatty Acids, Monounsaturated; D006538:Heptanoic Acids; D007211:Indoles; D011758:Pyrroles; D000077340:Fluvastatin; D008315:Malondialdehyde; D002784:Cholesterol; D000069059:Atorvastatin; D019821:Simvastatin; D017035:Pravastatin