title: Relationship between oxidative stress, lipid peroxidation, and ultrastructural damage in patients with coronary artery disease undergoing cardioplegic arrest/reperfusion.
abstract: OBJECTIVE
  In animal models, formation of oxidants during postischemic reperfusion may exert deleterious effects ("oxidative stress"). Cardioplegic arrest/reperfusion during cardiac surgery might similarly induce oxidative stress. However, the phenomenon has not been precisely characterized in patients, and therefore the role of antioxidant therapy at cardiac surgery is a matter of debate. Thus, we wanted to ascertain whether the relationship between oxidant formation and development of myocardial injury also translates to the situation of patients subjected to cardioplegic arrest.
  
  
  METHODS
  In 24 patients undergoing coronary artery bypass, trans-cardiac blood samples and myocardial biopsies were taken before cardioplegic arrest and again following reperfusion.
  
  
  RESULTS
  Cardiac glutathione release (marker of oxidant production) was negligible at baseline (0.02+/-0.04 micromol/L), but it increased 15 min into reperfusion (1.10+/-0.40 micromol/L; p<0.05); concomitantly, myocardial concentration of the antioxidant ubiquinol decreased from 144.5+/-52.0 to 97.6+/-82.0 nmol/g (p<0.05). Although these changes document cardiac exposure to oxidants, they were not accompanied by evidence of injury. Neither coronary sinus blood nor cardiac biopsies showed increased lipid peroxide concentrations. Furthermore, electron microscopy showed no major ultrastructural alterations. Finally, full recovery of left ventricular systolic and diastolic function was observed.
  
  
  CONCLUSIONS
  Careful investigation reveals that while oxidant production does occur during cardiac surgery in patients with chronic ischemic heart disease, cardiac oxidative stress may not progress through membrane damage and irreversible injury.
authors.affiliation: Instituto de Investigaciones Cardiológicas Alberto C. Taquini UBA-Conicet, Buenos Aires, Argentina.
authors.forename: José
authors.initials: J
authors.lastname: Milei
authors.forename: Pedro
authors.initials: P
authors.lastname: Forcada
authors.forename: César G
authors.initials: CG
authors.lastname: Fraga
authors.forename: Daniel R
authors.initials: DR
authors.lastname: Grana
authors.forename: Gabriele
authors.initials: G
authors.lastname: Iannelli
authors.forename: Massimo
authors.initials: M
authors.lastname: Chiariello
authors.forename: Isabella
authors.initials: I
authors.lastname: Tritto
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Ambrosio
mesh_terms: D000368:Aged; D000704:Analysis of Variance; D015415:Biomarkers / Q000097:blood; D002315:Cardiopulmonary Bypass / Q000009:adverse effects*; D001026:Coronary Artery Bypass / Q000009:adverse effects*; D003324:Coronary Artery Disease / Q000378:metabolism / Q000473:pathology / Q000601:surgery*; D005260:Female; D005978:Glutathione / Q000097:blood; D006801:Humans; D007432:Intraoperative Period; D015227:Lipid Peroxidation; D008297:Male; D008854:Microscopy, Electron; D008875:Middle Aged; D008929:Mitochondria, Heart / Q000648:ultrastructure; D017202:Myocardial Ischemia / Q000378:metabolism / Q000473:pathology; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000737:chemistry / Q000378:metabolism* / Q000648:ultrastructure; D016877:Oxidants; D018384:Oxidative Stress; D011184:Postoperative Period; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis
chemical_list: D015415:Biomarkers; D016877:Oxidants; D017392:Thiobarbituric Acid Reactive Substances; D005978:Glutathione