ABSTRACT
Objective To investigate the effect of propofol on autophagy in SD rat heart during myocar-dial ischemia-reperfusion (I/R) injury. Methods Twenty-one male SD rats were randomly divided into three groups as follows (n = 7): the sham operation group, in which rats underwent sham operation without tightening of the coronary artery sutures; the myocardial ischemia-reperfusion group , in which rats were induced by occlud-ing the left anterior descending coronary artery for 30 min , followed by 120 min reperfusion and 0.9% NaCl in-fusion at 3 mL/(kg·h) at 10 min before occluding the left anterior descending coronary artery; the myocardial ischemia- reperfusion- propofol group, in which rats underwent I/R and propofol infusion at 6 mg/(kg·h) at 10 min before occluding the left anterior descending coronary artery. Before tightening of the coronary artery, at 30 min post-tightening of the coronary artery and at 120 min post-reperfusion, HR、 LVSP and ± dp/dtmax of rats were recordedin each group. Atter 120 min post-reperfusion, the serum concentrations of cTnT was measured. The in-jured cardiac tissue was collected to investigate the ultrastructure change under the TEM and to determine the levels of mTOR and p-mTOR. Results No signifcant differences in HR, LVSP and ± dp/dtmax before tighten-ing of the coronary artery. But, at 30 min post- tightening of the coronary artery, compared with groupⅠ, the HR, LVSP and ±dp/dtmax were significantly decresed in groupⅡ and Ⅲ(P < 0.05). Then, at 2 h post-reper-fusion, compared with groupⅠ, the HR, LVSP, ±dp/dtmax and the level of p-mTOR were significantly de-creased, but the serum concentration of cTnT was significantly increased in groupⅡ(P < 0.05); but, compared with groupⅡ, the HR, LVSP, ± dp/dtmax and the level of p-mTOR were significantly increased, the serum concentration of cTnT and the level of mTOR were significantly decreased in group Ⅲ(P < 0.05). Conclusions These data suggest that propofol could heighten the level of p-mTOR, and attenuate the expression of mTOR dur-ing the myocardial ischemia-reperfusion injury in SD rats.