title: Ischemic preconditioning improves preservation with cold blood cardioplegia in valve replacement patients.
abstract: OBJECTIVE
  The purpose of this study was to test the hypothesis that ischemic preconditioning improves myocardial protection in valve replacement patients undergoing cold-blood cardioplegic arrest and to study the mechanisms of human myocardial ischemic preconditioning initially.
  
  
  METHODS
  Forty patients who required double valve replacement were studied. After the institution of cardiopulmonary bypass, 20 patients were preconditioned with two cycles of 3 min of aortic cross-clamping and 2 min of reperfusion before cardioplegic arrest (group IP). Twenty patients were not preconditioned as controls (group C). All hearts were arrested with 4 degrees C cold-blood cardioplegic solution. During perioperation, the blood samples were collected from coronary sinus and radial artery, which were used to measure calcitonin gene-related peptide (CGRP) and creatine kinase-MB (CK-MB). The right atrial myocardial tissue was collected to measure superoxide dismutase/malondialdehyde (T-SOD/MDA) and to observe myocardial ultrastructure. Hemodynamic date were measured.
  
  
  RESULTS
  After reperfusion for 30 min, myocardial MDA was significantly lower in group IP than in group C (2.6+/-0.2 vs. 3.8+/-0.3 nM/mg) and T-SOD was significantly higher in group IP than in group C (13.1+/-12.1 vs. 9.2+/-1.2 IU/mg). Ischemic preconditioning significantly increased the production of myocardial CGRP just after preconditioning (92.0+/-4.1 vs. 52.3+/-4.5 pg/ml) and the begin of reperfusion (95.3+/-3.8 vs. 61.2+/-4.9 pg/ml), and deduced the release of CK-MB at 12 h post-reperfusion (77.5+/-9.2 vs. 136.5+/-8.9 IU/l). Preconditioning also improved cardiac function at 30 min and 12 h after reperfusion (cardiac index 2.8+/-0.3 vs. 2.3+/-0.2 l/min per m2 and 2.9+/-0.1 vs. 2.4+/-0.2 l/min per m2).
  
  
  CONCLUSIONS
  Ischemic preconditioning enhance cardioplegic protection in valve replacement patients. The possible protective mechanism was that ischemic preconditioning decreased the production of oxygen free radicals.
authors.affiliation: Department of Cardiothoracic Surgery, Xiangya Hospital, Hunan Medical University, Changsha, Hunan, PR China. guohu-li@public.cs.hn.cn
authors.forename: G
authors.initials: G
authors.lastname: Li
authors.forename: S
authors.initials: S
authors.lastname: Chen
authors.forename: E
authors.initials: E
authors.lastname: Lu
authors.forename: Y
authors.initials: Y
authors.lastname: Li
mesh_terms: D000328:Adult; D005260:Female; D005500:Follow-Up Studies; D006324:Heart Arrest, Induced / Q000379:methods*; D006349:Heart Valve Diseases / Q000601:surgery*; D019918:Heart Valve Prosthesis Implantation / Q000379:methods*; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D019157:Ischemic Preconditioning, Myocardial / Q000379:methods*; D008297:Male; D009206:Myocardium / Q000473:pathology; D011446:Prospective Studies; D012016:Reference Values; D016896:Treatment Outcome