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目的观察异丙酚对心肌缺血再灌注损伤大鼠离体心脏脂质代谢的影响。方法雄性Wistar大鼠68只,体重350-450 g,随机分为2组(n=34):正常对照组(C组)和心肌缺血再灌注组(I/ R组)。I／R组阻断左冠状动脉前降支,缺血30 min,再灌注2 h制备心肌缺血再灌注模型,取心脏在Langendorff。灌注模型上用Krebs-Hemseleit(KBH)缓冲液灌注,将用放射性物质标记的(TAG)0．4mol／L加入循环回路中。分别用含不同浓度异丙酚[0(生理盐水)、0．1、1．0、5．0、10．0、500μmol／L]的灌注液进行灌注,监测平均动脉压、心率、主动脉流量(AFR)、冠状动脉血流(CFR),计算Hydraulic work反映心肌作功情况。测定灌注液中TAG浓度,计算脂肪酸(FFA)氧化率,并测定心肌脂蛋白酶(LPL)活性。结果心肌缺血再灌可导致Hydraulic work降低,FFA氧化率和心肌LPL活性升高;与C组异丙酚浓度为0时比较,C组异丙酚浓度为10．0、50．0μmol／L时Hydraulic work降低,异丙酚浓度为5．0-50．0μmol／L时灌注液中TAG浓度升高,I／R组异丙酚浓度为10．0、50．0μmol／L时Hydraulic work降低,异丙酚浓度为5．0～50．0μmol／L时灌注液中TAG浓度升高,异丙酚浓度为10．0-50．0μmol／L时FFA氧化率和心肌LPL活性降低(P<0．05);与I／R组异丙酚浓度为0时比较,I／R组异丙酚浓度为0．1～10．0μmol／L时Hydraulic work升高,异丙酚浓度为5．0～50．0μmol／L时灌注液中TAG浓度升高,FFA氧化率及心肌LPL活性降低(P<0．05)。结论异丙酚可减轻心肌缺血再灌注损伤大鼠心脏功能的降低,其机制与改善心肌脂质代谢有关。
Objective To investigate the effect of propofol on lipid metabolism in isolated rat hearts with myocardial ischemia reperfusion injury. Methods Sixty-eight male Wistar rats weighing 350-450 g were randomly divided into two groups (n = 34): normal control group (C group) and myocardial ischemia reperfusion group (I / R group). The I / R group blocked the left anterior descending coronary artery, ischemia 30 min, reperfusion 2 h after myocardial ischemia reperfusion model, take the heart in Langendorff. Perfusion models were perfused with Krebs-Hemseleit (KBH) buffer and radioactively labeled (TAG) 0.4 mol / L was added to the circulation. The rats were perfused with different concentrations of propofol [0 (saline), 0.1, 1.0, 5.0, 10.0 and 500 μmol / L] respectively. The mean arterial pressure, heart rate, Flow rate (AFR), coronary blood flow (CFR), calculated hydraulic work reflects the work of the heart. The concentration of TAG in the perfusate was measured to calculate the fatty acid (FFA) oxidation rate, and the activity of cardiac lipoprotein (LPL) was measured. Results Myocardial ischemia / reperfusion resulted in the decrease of Hydraulic work and the increase of FFA oxidation rate and myocardial LPL activity. Compared with group C, the concentration of propofol in group C was 10.0 and 50.0 μmol / L The hydraulic work was decreased, the concentration of TAG in the perfusate increased when the concentration of propofol was 5.0-50.0 μmol / L, and the hydraulic work was decreased in the group of I / R propofol at 10.0 and 50.0 μmol / L , The concentration of TAG in perfusate increased with propofol concentration of 5.0-50.0μmol / L, the FFA oxidation rate and myocardial LPL activity decreased with propofol concentration of 10.0-50.0μmol / L (P < 0.05). Compared with I / R group, when Propofol concentration was 0, Propofol concentration was 0.1 ~ 10.0μmol / L in I / R group, and Hydraulic work was increased. Propofol concentration was 5. The concentration of TAG increased, FFA oxidation rate and myocardial LPL activity decreased (P <0.05) at 0-50.0μmol / L. Conclusion Propofol can reduce the cardiac function of myocardial ischemia-reperfusion injury in rats, and its mechanism is related to the improvement of myocardial lipid metabolism.