title: [Effect of remifentanil preconditioning on myocardial ischemia-reperfusion injury].
abstract: OBJECTIVE
  To investigate the delayed cardioprotection induced by remifentanil in intact rat ischemia-reperfusion (I/R) models.
  
  
  METHODS
  Totally 42 adult male Wistar rats weighing 200-300 g were randomly divided into 7 groups (n = 6 in each group): In Group I, rats were injected with normal saline via tail vein, performed with the regimen of 3 x 5-min intravenous (i.v.) infusion at a rate of 0.1 ml x kg(-1) min(-1) 24 h before I/R; In Group II, rats were treated according to the same experimental protocols as in Group I except receiving additional naloxone (0.1 mg/kg) 10 minutes before normal saline pretreatment; In Groups III, IV, V, and VI, rats were treated with remifentanil via tail vein, performed with the regime of 3 x 5-min i.v. infusion at a rate of 2 microg x kg(-1) x min(-1) 12 h, 24 h, 48 h, and 72 h before I/R; In Group VII, the rats were treated according to the same experimental protocols as in Group IV except that they received additional naloxone (0.1 mg/kg) 10 minutes before remifentanil pretreatment. Heart rate (HR), mean arterial pressure (MAP), and a lead II electrocardiogram were continuously monitored during IR process. To determine plasma concentration of creatine kinase myocardial isoenzyme-MB (CK-MB), arterial blood samples were obtained immediately before ischemia, and at the end of ischemia and reperfusion. After a 120-min reperfusion, heart was removed for the measurement of myocardial infarct size. Infarct size (IS) was expressed as percentage of the area at risk.
  
  
  RESULTS
  HR, MAP, and rate-pressure product were not significantly different at each time points among all groups (P > 0.05). Compared with Group I, plasma concentrations of CK-MB at the end of ischemia and reperfusion and myocardial infarct size were significantly lower in Groups IV and V (P < 0.05). Compared with Group IV, plasma concentrations of CK-MB at the end of ischemia and reperfusion were significantly higher and myocardial infarct size was significantly larger in Group VII (P < 0.05).
  
  
  CONCLUSIONS
  Remifentanil preconditioning induces delayed cardioprotection in intact rat ischemia-reperfusion model, which may be triggered via opioid receptors.
authors.affiliation: Department of Anesthesiology, Cancer Hospital and Institute, CAMS and PUMC, Beijing 100021, China.
authors.forename: Hai-Tao
authors.initials: HT
authors.lastname: Sun
authors.forename: Fu-Shan
authors.initials: FS
authors.lastname: Xue
authors.forename: Kun-Peng
authors.initials: KP
authors.lastname: Liu
authors.forename: Li
authors.initials: L
authors.lastname: Sun
authors.forename: Ya-Chao
authors.initials: YC
authors.lastname: Xu
authors.forename: Xu
authors.initials: X
authors.lastname: Liao
authors.forename: Quan-Yong
authors.initials: QY
authors.lastname: Yang
authors.forename: Yan-Ming
authors.initials: YM
authors.lastname: Zhang
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D019157:Ischemic Preconditioning, Myocardial; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology* / Q000517:prevention & control; D010880:Piperidines / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D000077208:Remifentanil
chemical_list: D010880:Piperidines; D000077208:Remifentanil