title: Noninvasive limb ischemic preconditioning protects against myocardial I/R injury in rats.
abstract: BACKGROUND
  Transient limb ischemia induces remote early preconditioning that protects the myocardium from ischemia/reperfusion (I/R). However, it is unknown whether limb ischemia induces remote late preconditioning and whether it induces the same magnitude of cardioprotection compared with cardial ischemic preconditioning (CIP). We tested the hypothesis that late remote preconditioning of noninvasive limb ischemia (NLIP) offers the same magnitude of cardioprotection against myocardium I/R injury.
  
  
  METHODS
  Thirty Wistar rats weighing 240-260 g each were randomly divided into three groups: I/R, CIP, and NLIP. The mean arterial pressure (MAP), heart rate (HR), ST-segment, ventricular arrhythmia, and CK-MB, cTnI, and superoxide dismutase (SOD) activity were measured after 0 and 30 min of ischemia and after 120 min of reperfusion. Myocardial infarct size, histologic examination, MMP-2, MMP-9, and TIMP-1 protein expression were determined at the end of the experiment.
  
  
  RESULTS
  Compared with I/R groups, CIP and NLIP reduced ST-segment elevation (P<0.01), decreased incidence and duration of ventricular arrhythmia (P<0.01) during ischemia, decreased CK-MB (P<0.05), and cTnI (P<0.01) activity, and increased SOD (P<0.05) activity after reperfusion. The myocardial infarct size (P<0.01) was significantly reduced, and cell injury was attenuated in the CIP and NLIP groups compared with the I/R group. MMP-2 and MMP-9 protein expression was significantly decreased in the CIP and NLIP groups (P<0.01), while TIMP-1 expression was significantly increased in the CIP and NLIP groups compared with the I/R group (P<0.01).
  
  
  CONCLUSIONS
  Remote preconditioning via NLIP has late cardioprotection against myocardium I/R injury and has a similar magnitude of cardioprotection compared with CIP in rats.
authors.affiliation: Department of Pharmacology, Tianjin Medical University, Tianjin, PR China.
authors.forename: Shu-Juan
authors.initials: SJ
authors.lastname: Li
authors.forename: Yan-Na
authors.initials: YN
authors.lastname: Wu
authors.forename: Yi
authors.initials: Y
authors.lastname: Kang
authors.forename: Yong-Qiang
authors.initials: YQ
authors.lastname: Yin
authors.forename: Wei-Zhen
authors.initials: WZ
authors.lastname: Gao
authors.forename: Yan-Xia
authors.initials: YX
authors.lastname: Liu
authors.forename: Jian-Shi
authors.initials: JS
authors.lastname: Lou
mesh_terms: D000818:Animals; D001794:Blood Pressure; D052279:Creatine Kinase, MB Form / Q000097:blood; D004562:Electrocardiography; D006339:Heart Rate; D006614:Hindlimb / Q000098:blood supply*; D019157:Ischemic Preconditioning, Myocardial / Q000379:methods*; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000097:blood; D020780:Matrix Metalloproteinase 9 / Q000097:blood; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000097:blood; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000097:blood; D019210:Troponin I / Q000097:blood
chemical_list: D019715:Tissue Inhibitor of Metalloproteinase-1; D019210:Troponin I; D013482:Superoxide Dismutase; D052279:Creatine Kinase, MB Form; D020778:Matrix Metalloproteinase 2; D020780:Matrix Metalloproteinase 9