Effect of sevoflurane postconditioning on expression of optic atrophy-1 during myocardial ischemia-reperfusion in rats

Objective To evaluate the effect of sevoflurane postconditioning on expression of optic atrophy-1 (OPAl) during myocardial ischemia-reperfusion (I/R) in rats.Methods Forty-five healthy adult male Sprague-Dawley rats,aged 3 months,weighing 220-280 g,were randomly divided into 3 groups (n =15 each) using a random number table:sham operation group (group S),ischemia-reperfusion group (group I/R),and sevoflurane postconditioning group (group SP).Myocardial ischemia was induced by 30 min occlusion of left anterior descending branch of coronary artery followed by 120 min reperfusion.2.5 ％ sevoflurane was inhaled for 5 min starting from 29 min of ischemia until 4 min after beginning of reperfusion in SP group,while 33 ％ oxygen was inhaled in the other groups.Heart rate,systolic pressure and mean arterial pressure (MAP) were monitored and recorded and rate-pressure product (RPP) was calculated at 15 min before ischemia (T0),15 min of ischemia (T1),and 60 and 120 min of reperfusion (T2,3).At the end of reperfusion,the rats were sacrificed and the hearts were removed for determination of myocardial infarct size.The expression of OPAl mRNA and protein was measured by RT-PCR and immunohistochemistry,respectively.Their hearts were cut into sections which were stained with H.E.and examined under light microscope.Morphological changes of mitochondria were examined by electron microscopy.Results Compared with group S,MAP and RPP were significantly decreased at T1-3,the expression of OPA1 mRNA and protein was down-regulated,and the myocardial infarct size was increased in I/R and SP groups.Compared with group I/R,MAP and RPP were significantly decreased at T2,3,the expression of OPA1 mRNA and protein was up-regulated,and the myocardial infarct size was decreased in group SP.Conclusion Sevoflurane postconditioning can reduce myocardial I/R injury through up-regulating myocardial OPA1 expression,protecting mitochondrial morphology and inhibiting apoptosis in cardiomyocytes of rats. Key words: Anesthetics, inhalation;  Myocardial reperfusion injury;  Optic atrophy-1;  Ischemic postconditioning