title: Free radicals, antioxidants, and endothelial cell damage after percutaneous transluminal coronary angioplasty.
abstract: BACKGROUND
  Oxygen-derived free radicals (ODFRs) and subsequent lipid peroxidation may be responsible for myocardial damage associated with ischaemia/reperfusion after percutaneous transluminal coronary angioplasty (PTCA). These potentially cytotoxic ODFRs are likely to be generated in the plasma, where the primary target organ or cell may be the endothelium. Some of these toxic effects may be limited by the action of antioxidant enzymes such as glutathione peroxidase (GPx). The aim of this study was to determine whether there was evidence of ODFR-mediated damage to the endothelium after PTCA and to examine the roles of lipid peroxides and GPx.
  
  
  METHODS
  Serial samples of plasma were obtained at the time of catheter insertion, at the time of balloon inflation, 10 min after inflation, and 60 min after inflation, from 16 patients undergoing PTCA. We measured levels of von Willebrand factor (vWf, a specific product of the endothelium and a marker of damage), thiobarbituric acid reactive substances (TBARS, an indirect measure of the activity of ODFRs in peroxidizing lipoproteins), and the antioxidant GPx.
  
  
  RESULTS
  There was a simultaneous peak in the levels of TBARS (P = 0.0096) with a fall in the levels of GPx (P = 0.004) 10 min after balloon deflation. Sixty min after balloon deflation, GPx levels were still reduced (P = 0.005) but there was a rise in levels of vWf (P = 0.038).
  
  
  CONCLUSIONS
  Our interpretation of these data is that an early peak in ODFR activity associated with PTCA causes an endothelial injury 1 h after inflation. This may be related to the reduced ability of GPx to scavenge ODFRs.
authors.affiliation: Department of Surgery, University Hospital of South Manchester, UK.
authors.forename: A
authors.initials: A
authors.lastname: Blann
authors.forename: H
authors.initials: H
authors.lastname: Midgley
authors.forename: G
authors.initials: G
authors.lastname: Burrows
authors.forename: S
authors.initials: S
authors.lastname: Maxwell
authors.forename: S
authors.initials: S
authors.lastname: Utting
authors.forename: M
authors.initials: M
authors.lastname: Davies
authors.forename: M
authors.initials: M
authors.lastname: Waite
authors.forename: C
authors.initials: C
authors.lastname: McCollum
mesh_terms: D000328:Adult; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D000975:Antioxidants / Q000378:metabolism; D003327:Coronary Disease / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology*; D005260:Female; D005979:Glutathione Peroxidase / Q000502:physiology*; D006801:Humans; D015227:Lipid Peroxidation / Q000502:physiology; D008297:Male; D008875:Middle Aged; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000473:pathology* / Q000503:physiopathology; D017382:Reactive Oxygen Species / Q000378:metabolism*; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D013997:Time Factors; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D000975:Antioxidants; D017382:Reactive Oxygen Species; D017392:Thiobarbituric Acid Reactive Substances; D014841:von Willebrand Factor; D005979:Glutathione Peroxidase