[Effect of isoflurane delayed preconditioning on the expression of Bcl-2 and caspase-3 in myocardium during ischemia reperfusion in rabbits].

OBJECTIVE: To investigate the effect of isoflurane delayed preconditioning on the activation of caspase-3 and the expression of Bcl-2 in rabbit myocardium during ischemia reperfusion and the possible mechanism. METHODS: Forty New Zealand male white rabbits were randomly divided into 4 groups: a sham group (Group C), an I/R group, an isoflurane group (Group S), and an isoflurane + opioid recepters inhibitor group (Group N). Group S was exposed to 2.0% isoflurane for 2 h. Group N was given naloxone (6.0 mg/kg) before exposing to 2.0% isoflurane. Group C and Group I/R were exposed for 2 h to 100% oxygen, serving as untreated controls. Twenty-four hours later, Group S and Group N underwent 40 min of coronary occlusion followed by 2 h of reperfusion. At the end of the reperfusion, infarct size(IS) and area at risk(AAR) were defined by Evans and TTC staining. The myocardial ultrastructure was observed by electron microscopy. The levels of the myocardial Bcl-2 and caspase-3 expression were determined by Western blot. RESULTS: The caspase-3 activity of Group S was significantly lower than that of Group I/R(P<0.05). The IS was significantly reduced in Group S(19.7%+/-2.8%) as compared with Group I/R(37.8%+/-1.7%) (P<0.05). Microscopic examination showed less myocardial damage in Group S than in Group I/R. CONCLUSION: Isoflurane delayed preconditioning can inhibit the apoptosis of myocardium by up-regulating the expression of Bcl-2 and down-regulating the activation of caspase-3, which may be part of the molecular mechanism of isoflurane delayed preconditioning on myocardial preservation.