title: Oxidative stress implication after prolonged storage donor heart with blood versus crystalloid cardioplegia and reperfusion versus static storage.
abstract: Several factors are known to limit cardiac transplantation, such as number of donors, quality of cardiac graft preservation, and ischemia-reperfusion injury. Some mechanisms of reperfusion injury are now recognized; they include oxygen free radical (OFR), white blood cells activation, changes in calcium influx, alteration of microvascular blood flow, and sympathetic activation. The goal of this study was to assess the effects of two types of cardioplegia with long-term storage, either static or continuous perfusion, in 30 isolated sheep hearts as a model for heart transplantation. We examined myocardial function, histology, ischemic damage, and markers of oxidative stress. Two types of cardioplegia and storage conditions using a Langendorff reperfusion were studied in a combined approach: crystalloid (CP) [groups I and III] or cold oxygenated autologous blood (BC) [groups II and IV], immediate storage during 8h in profound hypothermia (groups I and II), or reperfused with crystalloid (group III), or blood cardioplegia (group IV). All perfusate samples were drawn from the coronary sinus. Lactate levels increased progressively in groups I, II, and IV, but not in group III, as no significant elevation was shown [90 min: 13.6+/-1.7 versus 5.2+/-1.0 mmol/L (P<0.01)]. Arrhythmias were more frequent when using BC (n=5) than CP (n=0). For plasma thiobarbituric acid-reactive substances (TBARS) levels a significant difference was found between group III and the other groups since 15 to 90 min (P<0.05). Vitamin E concentration decreased significantly from 5 min for groups II and IV, 15 min for group I, and 30 min for group III, with a significant difference between groups II and IV (P<0.05) but not between groups I and III. CP followed by a reperfusion with the same solution showed a significantly lower ischemic injury and OFR production, less frequent ventricular arrhythmias while stable hemodynamic parameters carried on. However, this protocol did not act on the early postoperative contractile function.
authors: Department of Cardiology, AP-HP Avicenne Hospital, Université Paris 13, Bobigny, France. jean-christophe.charniot@avc.aphp.fr
authors: Jean-Christophe
authors: JC
authors: Charniot
authors: Dominique
authors: D
authors: Bonnefont-Rousselot
authors: Jean-Paul
authors: JP
authors: Albertini
authors: Sylvie
authors: S
authors: Dever
authors: Noelle
authors: N
authors: Vignat
authors: Patrick
authors: P
authors: Nataf
authors: Alain
authors: A
authors: Pavie
authors: Jean-Jacques
authors: JJ
authors: Monsuez
authors: Jacques
authors: J
authors: DeLattre
authors: Jean-Yves
authors: JY
authors: Artigou
mesh_terms: D000818:Animals; D001145:Arrhythmias, Cardiac / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control; D001804:Blood Transfusion, Autologous; D015925:Cryopreservation / Q000379:methods; D005979:Glutathione Peroxidase / Q000378:metabolism; D006085:Graft Survival; D006324:Heart Arrest, Induced / Q000379:methods; D016027:Heart Transplantation; D019344:Lactic Acid / Q000378:metabolism; D015227:Lipid Peroxidation; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D009926:Organ Preservation / Q000379:methods*; D018384:Oxidative Stress / Q000187:drug effects*; D017680:Potassium Compounds / Q000494:pharmacology*; D015427:Reperfusion Injury / Q000378:metabolism* / Q000473:pathology / Q000517:prevention & control; D012756:Sheep; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D017725:Ventricular Pressure; D014801:Vitamin A / Q000378:metabolism; D014810:Vitamin E / Q000378:metabolism; D019207:beta Carotene / Q000378:metabolism
chemical_list: D017680:Potassium Compounds; D017392:Thiobarbituric Acid Reactive Substances; C018369:potassium cardioplegic solution; D019207:beta Carotene; D014801:Vitamin A; D014810:Vitamin E; D019344:Lactic Acid; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase