title: Effects of acute and chronic atorvastatin on cardioprotection of ischemic postconditioning in isolated rat hearts.
abstract: BACKGROUND
  Myocardial reperfusion therapy remains the most effective strategy to limit infarct size and improve clinical outcome. However, reperfusion injury is still inevitable, and a number of strategies have been developed to ameliorate its lethal outcome. The beneficial roles of ischemic postconditioning (Ipost) have regained more interest in targeting myocardial reperfusion phase to improve cardioprotection.
  
  
  OBJECTIVE
  This study was to determine whether acute or chronic treatment with atorvastatin affects cardioprotection when it was combined with Ipost.
  
  
  RESULTS
  Acute or chronic atorvastatin treatment significantly reduced infarct size and recovered contractile dysfunction during reperfusion. When Ipost was combined with atorvastatin treatment, chronic, but not acute, atorvastatin therapy attenuated the cardioprotective effects of Ipost. Chronic, but not acute, atorvastatin treatment also abolished Ipost-induced phosphorylation level of Akt and endothelial nitric oxide synthase (eNOS).
  
  
  CONCLUSIONS
  Chronic atorvastatin treatment could interfere with cardioprotective effects of Ipost on limiting infarct size and contractile dysfunction, possibly via inhibition of Akt and eNOS activity. This study suggests that Ipost should be used carefully when atorvastatin is taken by patients with AMI.
authors.affiliation: Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, Heilongjiang, China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Fan
authors.forename: Shusen
authors.initials: S
authors.lastname: Yang
authors.forename: Yang
authors.initials: Y
authors.lastname: Cao
authors.forename: Yonglin
authors.initials: Y
authors.lastname: Huang
mesh_terms: D000818:Animals; D000069059:Atorvastatin; D002316:Cardiotonic Agents / Q000008:administration & dosage*; D004334:Drug Administration Schedule; D006439:Hemodynamics / Q000187:drug effects; D006538:Heptanoic Acids / Q000008:administration & dosage*; D066298:In Vitro Techniques; D057775:Ischemic Postconditioning; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D011758:Pyrroles / Q000008:administration & dosage*; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction / Q000187:drug effects; D013997:Time Factors
chemical_list: D002316:Cardiotonic Agents; D006538:Heptanoic Acids; D011758:Pyrroles; D000069059:Atorvastatin; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat; D051057:Proto-Oncogene Proteins c-akt