title: Effect of acute changes in oxygen tension on flow-mediated dilation. Relation to cardivascular risk.
abstract: OBJECTIVE
  Oxygen-dependent changes in vascular diameters may be detrimental when the endothelium is dysfunctional.
  
  
  METHODS
  Endothelial responsiveness was evaluated by brachial ultrasound and flow-mediated/nitroglycerin-mediated dilation (FMD/NMD). FMD/NMD was investigated in males with increased risk of cardiovascular disease (mean age 44+/-2 years, n=10) and matched controls without risk factors (44+/-2 years, n=10). FMD/NMD was assessed during normoxia (21% O2, 79% N2), while inhaling hypoxic gas (12.5% O2, FMDHyp/NMD), and 100% O2 supplementation (FMDO2/NMD). In a second study we addressed the effect of lipid lowering. Twenty persons with cardiovascular risk (mean age 50+/-2 years) were treated with atorvastatin (80 mg/day) and FMD/NMD was measured during normoxia, hypoxia and oxygen supplementation before, after 1 day and 3 months.
  
  
  RESULTS
  Oxygen supplementation evoked vasoconstriction, while FMDHyp/NMD was reduced compared to FMD/NMD. Atorvastatin significantly lowered total cholesterol, LDL cholesterol, and ADMA after 1 day of treatment, while triglycerides, ApoB and hsCRP were lowered after 3 months. Atorvastatin did not change FMD/NMD irrespective of oxygen tension.
  
  
  CONCLUSIONS
  Irrespective of risk factors or atorvastatin, hypoxia reduced endothelial vasodilation while oxygen supplementation evoked vasoconstriction.
authors.affiliation: Center for Cardiovascular Research, Department of Cardiology, Aalborg Hospital, and Department of Pharmacology, University of Aarhus, Aalborg, Denmark. frobert@dadlnet.dk
authors.forename: Ole
authors.initials: O
authors.lastname: Frøbert
authors.forename: Pernille
authors.initials: P
authors.lastname: Holmager
authors.forename: Ken Michael
authors.initials: KM
authors.lastname: Jensen
authors.forename: Erik Berg
authors.initials: EB
authors.lastname: Schmidt
authors.forename: Ulf
authors.initials: U
authors.lastname: Simonsen
mesh_terms: D000280:Administration, Inhalation; D000328:Adult; D000069059:Atorvastatin; D001916:Brachial Artery / Q000187:drug effects / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000097:blood / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control; D002784:Cholesterol / Q000097:blood; D004730:Endothelium, Vascular / Q000000981:diagnostic imaging / Q000187:drug effects / Q000503:physiopathology*; D005260:Female; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D006938:Hyperlipoproteinemia Type II / Q000097:blood / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology; D018496:Hyperoxia / Q000503:physiopathology; D000860:Hypoxia / Q000503:physiopathology; D008074:Lipoproteins / Q000097:blood; D008297:Male; D008875:Middle Aged; D005996:Nitroglycerin / Q000008:administration & dosage; D010100:Oxygen / Q000008:administration & dosage*; D011758:Pyrroles / Q000627:therapeutic use*; D012039:Regional Blood Flow; D012107:Research Design; D012307:Risk Factors; D016896:Treatment Outcome; D014280:Triglycerides / Q000097:blood; D014463:Ultrasonography; D014661:Vasoconstriction / Q000187:drug effects*; D014664:Vasodilation / Q000187:drug effects*; D014665:Vasodilator Agents / Q000008:administration & dosage
chemical_list: D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008074:Lipoproteins; D011758:Pyrroles; D014280:Triglycerides; D014665:Vasodilator Agents; D002784:Cholesterol; D000069059:Atorvastatin; D005996:Nitroglycerin; D010100:Oxygen