title: [Effects of rabbit limbs ischemia/ reperfusion on myocardial necrosis and apoptosis].
abstract: OBJECTIVE
  To investigate the effects of rabbit limbs ischemia/reperfusion on myocardial necrosis and apoptosis in vivo.
  
  
  METHODS
  Thirty-six healthy new zealand rabbits were randomly divided into 3 groups: (1) Sham group; (2) I/R(Ischemia/reperfusion) group; (3) RPostC (remote postconditioning) group. The activity of blood serum creatine kinase (CK) and lactate dehydrogenase (LDH) were measured at baseline, the end of ischemia after 60 min and 120 min of reperfusion respectively. The extent of myocardial ischemia and the scope of myocardial infarction were assessed by evans blue and Triphenyl tetrazolium chloride (TTC). The myocardial cell's apoptosis at the area of myocardial ischemia was estimated by Tunel. Protein expression of caspase-3, Bcl-2 and Bax in myocardial ischemic area were analyzed with the method of immunohistochemistry.
  
  
  RESULTS
  Compared with I/R group, the myocardial infarct size and the CK activity were significantly reduced in RPostC group. The Tunel positive index of RPostC group in ischemic myocardium was significantly lower than that in I/R group (21.79% +/- 1.07% vs 35.81% +/- 1.10%, P < 0.05). Caspase-3 positive cells index was calculated with randomly selected five regions in each slide and then the positive cells in per hundred cells were calculated. The RPostC group of caspase-3 positive cells was significantly lower than that in I/ R group(25.03% +/- 1.16% as 39% +/- 2.43%, P < 0.05). Compared with the sham group, the Bax protein expression index and the Bcl-2 protein expression index of I/R group and RPostC group were increased. The Bax/Bcl-2 ratio of RPostC group decreased, while it was increased in I/R. Compared with the I/R group, the Bax protein expression and Bax/Bcl-2 ratio of RPostC group significantly reduced, but the expression index of Bcl-2 ratio was significantly increased, the differences were statistically significant.
  
  
  CONCLUSIONS
  Limbs ischemia/postconditioning could significantly reduce necrosis and apoptosis of ischemia/reperfusion myocardium. The mechanism of reducing the myocardial cell apoptosis may have relation to inhibiting the activation of pro-apoptotic gene caspase-3 and increased expression of Bcl-2.
authors.affiliation: Department of Cardiology, Hebei Medical University the Second Hospital, Shijiazhuang 050000, China.
authors.forename: Hui-Min
authors.initials: HM
authors.lastname: Ren
authors.forename: Rui-Qin
authors.initials: RQ
authors.lastname: Xie
authors.forename: Wei
authors.initials: W
authors.lastname: Cui
authors.forename: Fan
authors.initials: F
authors.lastname: Liu
authors.forename: Hai-Juan
authors.initials: HJ
authors.lastname: Hu
authors.forename: Jing-Chao
authors.initials: JC
authors.lastname: Lu
mesh_terms: D000818:Animals; D017209:Apoptosis; D053148:Caspase 3 / Q000378:metabolism; D003402:Creatine Kinase / Q000097:blood; D057775:Ischemic Postconditioning; D007770:L-Lactate Dehydrogenase / Q000097:blood; D035002:Lower Extremity; D008297:Male; D018482:Muscle, Skeletal / Q000098:blood supply; D015428:Myocardial Reperfusion Injury / Q000473:pathology*; D009336:Necrosis; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D011817:Rabbits; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase; D053148:Caspase 3