title: [Sevoflurane postconditioning attenuates myocardial apoptosis in isolated rat hearts via a modulation of Bcl-2 family proteins].
abstract: OBJECTIVE
  To explore the effects of sevoflurane postconditioning on ischemic/reperfused myocardial apoptosis.
  
  
  METHODS
  Isolated perfused rat hearts were randomly assigned into 3 groups: sham-operation (sham), ischemia/reperfusion (I/R) and sevoflurane postconditioning (SPC). Except for the sham group, the hearts were subjected to 40 min global myocardial ischemia and 120 min reperfusion. Left ventricular systolic pressure (LVSP), left ventricular developed pressure (LVDP), left ventricular end-diastolic pressure (LVEDP), maximum increase rate of LVDP (+dp/dt), maximum decrease rate of LVDP (-dp/dt), heart rate (HR) and coronary flow (CF) were measured at baseline, R (reperfusion) 30 min, R60 min, R90 min and R120 min. Creatine kinase (CK) and lactate dehydrogenase (LDH) were measured at 5 min and 10 min post-reperfusion. Infarct size was determined by triphenyltetrazolium chloride staining at the end of reperfusion. The expressions of Bcl-2 and Bax were determined by Western blot.
  
  
  RESULTS
  The values of LVSP, LVDP, ± dp/dt and CF were higher while that of LVEDP was lower in the SPC group than the I/R group at all time points of reperfusion (P < 0.05). The releases of CK and LDH and infarct size were significantly reduced in the SPC group versus the I/R group (22.2% ± 2.8% vs I/R: 44.9% ± 6.6%, P < 0.05). The expression of Bcl-2 increased significantly while that of Bax decreased in the SPC group verus the I/R group.
  
  
  CONCLUSIONS
  Sevoflurane postconditioning may improve myocardial functions, reduce infarct size and attenuate myocardial apoptosis. And the modulated expression of apoptotic proteins plays an important role in sevoflurane-induced myocardial protection.
authors.affiliation: Department of Anesthesiology, Zhejiang University, Hangzhou, China.
authors.forename: Li-na
authors.initials: LN
authors.lastname: Yu
authors.forename: Jing
authors.initials: J
authors.lastname: Yu
authors.forename: Feng-jiang
authors.initials: FJ
authors.lastname: Zhang
authors.forename: Mei-juan
authors.initials: MJ
authors.lastname: Yang
authors.forename: Wei
authors.initials: W
authors.lastname: He
authors.forename: Min
authors.initials: M
authors.lastname: Yan
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D066298:In Vitro Techniques; D008297:Male; D008738:Methyl Ethers / Q000494:pharmacology*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000517:prevention & control; D009206:Myocardium / Q000378:metabolism*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D000077149:Sevoflurane; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: C494828:Bax protein, rat; D008738:Methyl Ethers; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D000077149:Sevoflurane