title: [Propofol provides ischemic postconditioning on myocardial ischemia-reperfusion injury in rats].
abstract: OBJECTIVE
  To investigate whether the infusion of propofol during early reperfusion provides ischemic postconditioning (I-postC) on myocardial ischemia-reperfusion injury in rats.
  
  
  METHODS
  Sixty adult rats were randomly divided into 5 groups (n = 12 each): sham operation (group S); normal saline (group C); propofol 1 mg/kg (group P1); propofol 2 mg/kg (group P2); propofol 5 mg/kg (group P3). The left anterior descending coronary artery (LAD) was occluded for 60 min and reperfused for 120 min. Normal saline, propofol 1 mg/kg, 2 mg/kg or 5 mg/kg (propofol diluted to 2.5 ml with normal saline equally) were intravenously infused 3 min before reperfusion until 5 min after reperfusion. The heart were obtained for determination of (1) the size of area at risk and infarct size (Evans Blue and TTC staining); (2) expression of Caspase-3 (immunohistochemistry staining); (3) percentage of apoptotic cardiomyocytes (flow cytometry); (4) levels of phosphorylated Akt (Western blot).
  
  
  RESULTS
  Compared with group C [size of area at risk (41.5 +/- 1.0)%, infarct size (45.5 +/- 1.0)%, expression of caspase-3 (5.87 +/- 0.29), percentage of apoptotic cardiomyocytes (26.8 +/- 1.3)%, level of phosphorylated Akt (10.8 +/- 1.9)%], propofol 1 mg/kg and 2 mg/kg significantly reduced the size of area at risk and infarct size [size of area at risk (38.3 +/- 1.0)% and (37.3 +/- 1.2)%; infarct size (33.8 +/- 1.2)% and (30.2 +/- 1.7)%, P < 0.05], inhibited the expression of caspase-3 (1.50 +/- 0.36 and 1.48 +/- 0.30, P < 0.05), decreased the percentage of apoptotic cardiomyocytes [(16.3 +/- 1.2)% and (16.5 +/- 1.0)%, P < 0.05] and promoted the phosphorylation of Akt [(68.7 +/- 4.0)% and (58.3 +/- 2.8)%, P < 0.05].
  
  
  CONCLUSIONS
  Propofol 1 mg/kg and 2 mg/kg can provide I-postC to myocardial ischemia-reperfusion injury in rats by activation of Akt pathway.
authors.affiliation: Department of Anesthesiology, General Hospital, Tianjin Medical University, Tianjin 300052, China. wanghy819@yahoo.com.cn
authors.forename: Hai-Yun
authors.initials: HY
authors.lastname: Wang
authors.forename: Guo-Lin
authors.initials: GL
authors.lastname: Wang
authors.forename: Yong-Hao
authors.initials: YH
authors.lastname: Yu
authors.forename: Xing-Yun
authors.initials: XY
authors.lastname: Chen
authors.forename: Ying
authors.initials: Y
authors.lastname: Wang
mesh_terms: D000818:Animals; D017209:Apoptosis; D053148:Caspase 3 / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism / Q000517:prevention & control; D015742:Propofol / Q000627:therapeutic use*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar
chemical_list: D051057:Proto-Oncogene Proteins c-akt; D053148:Caspase 3; D015742:Propofol