title: Ischemic postconditioning promotes left ventricular functional recovery after cardioplegic arrest in an in vivo piglet model of global ischemia reperfusion injury on cardiopulmonary bypass.
abstract: OBJECTIVE
  An in vivo study of piglets on cardiopulmonary bypass was performed to determine whether postconditioning has a cardioprotective effect after cardioplegic arrest in large animals.
  
  
  METHODS
  Eighteen piglets were subjected to 90 minutes of cardioplegic arrest followed by 30 minutes of reperfusion. In 6 animals (control), there was no intervention at reperfusion. In 6 other animals, 6 cycles of unclamping and reclamping for 10 seconds each were done before reperfusion (postconditioning 10), whereas 3 cycles of unclamping and reclamping for 30 seconds each were performed in another 6 piglets (postconditioning 30).
  
  
  RESULTS
  Recovery of left ventricular contractility and diastolic function (percent of preischemic value) was significantly better in both postconditioning groups (contractility: 89.2% and 118.2; diastolic function: 142.3% and 120.4; in the postconditioning 10 and 30 groups, respectively) compared with the control (contractility: 46.1%; diastolic function: 218.5%). Recovery of global cardiac function (ventricular function curve analysis) was improved only in the postconditioning 30 group. Troponin-T release during reperfusion was significantly reduced in the postconditioning 10 group compared with all groups (plasma troponin-T was 0.58 ng/mL in postconditioning 10, 1.85 in postconditioning 30, and 2.54 in control). The myocardial lipid peroxide was significantly higher in the control group than in both postconditioning groups after reperfusion (199% vs 112% and 131%).
  
  
  CONCLUSIONS
  Both postconditioning algorisms promoted functional recovery after cardioplegic arrest in a large animal model along with the limitation of lipid peroxidation with or without the reduction of troponin-T release.
authors.affiliation: Department of Cardiac Surgery, Jikei University School of Medicine, Tokyo, Japan.
authors.forename: Gen
authors.initials: G
authors.lastname: Shinohara
authors.forename: Kiyozo
authors.initials: K
authors.lastname: Morita
authors.forename: Ryuichi
authors.initials: R
authors.lastname: Nagahori
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Koh
authors.forename: Katsushi
authors.initials: K
authors.lastname: Kinouchi
authors.forename: Takayuki
authors.initials: T
authors.lastname: Abe
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Hashimoto
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000097:blood; D002315:Cardiopulmonary Bypass / Q000009:adverse effects*; D004195:Disease Models, Animal; D006324:Heart Arrest, Induced / Q000009:adverse effects*; D057775:Ischemic Postconditioning; D015227:Lipid Peroxidation; D009200:Myocardial Contraction; D015428:Myocardial Reperfusion Injury / Q000097:blood / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism; D020127:Recovery of Function; D013552:Swine; D013997:Time Factors; D020107:Troponin T / Q000097:blood; D016277:Ventricular Function, Left
chemical_list: D015415:Biomarkers; D020107:Troponin T