Effect of sevoflurane preconditioning on cardiomyocyte apoptosis following myocardial ischemia/reperfusion in rats

Objective To investigate the effect of sevoflurane (Sero) preconditioning (Precon) on cardiomyocyte apoptosis following myocardial ischemia-reperfusion (I/R) in rats. Methods Sixty-four adult male SD rats weighing 270-350 g were randomly divided into 4 groups ( n = 16 each): group Ⅰ sham operation (group S); group Ⅱ myocardial I/R; group Ⅲ Sero and group Ⅳ Sevo-Precon + myocardial I/R. The animals were anesthetized with intraperitoneal pentobarbital 50 mg/kg, intubated and mechanically ventilated. PET CO2 was maintained at 35-45 mm Hg. Myocardial I/R was induced by 30 min occlusion of the left anterior descending branch of coronary artery followed by 2 h reperfusion in group Ⅱ and Ⅳ . In group Ⅲ the animals inhaled 2.5 % sevoflurane for 30 min while in group Ⅳ the animals inhaled 2.5% sevoflurane for 30 min at 15 min before myocardial I/R. Eight animals were killed at the end of 2 h reperfusion in each group. The hearts were removed for determination of myocardial infarct size (IS) as a percentage of area at risk (AAR) (IS/AAR) by triphenyl tetrazolium chloride staining. Myocardial apoptosis was detected using TUNEL and apoptosis index (AI) was calculated. Another 4 animals were killed before ischemia and at the end of 2 h reperfusion for determining the expression of Bcl-2 and caspase-3 protein in myocardium by Western blot. Results Sevoflurane preconditioning significantly decreased infarct size and AI in group Ⅳ as compared with group Ⅱ (group I/R). Bcl-2 protein expression was significantly decreased and caspase-3 protein expression was significantly increased after 2 h reperfusion as compared with the expression before ischemia in group I/R (group Ⅱ ). Sevoflurane preconditioning significantly reversed the I/R-induced changes in Bcl-2 and caspase-3 protein expression. Conclusion Sevoflurane preconditioning can attenuate myocardial I/R injury by decreasing myocardial apoptosis. Key words: Anesthetics, inhalation; Myocardial repeffusion injury; Apoptosis