摘要
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 different concentrations of propofol on myocardial lipid metabolism in isolated hearts after ischemia-reperfusion （I/R） and the underlying mechanism.Methods Sixtyeight male Wistar rats weighing 350-450 g were randomly divided into control group and I/R group. The animals were anesthetized with intraperitoneal （IP） phenobarbital 60 mg·kg^-1. In I/R group the anterior descending branch of left coronary artery was occluded for 30 min followed by 2 h reperfusion after thoracotomy. The hearts were then excised and passively perfused in a Langendorff apparatus with oxygenated Krebs-Henseleit buffer （KHB） at 37℃. A working Langendorff preparation was established by active perfusion of left atrium at 15 cm H2O through a catheter inserted via pulmonary vein into left atrium. Systolic BP, HR, aortic flow rate （AFR） and coronary flow rate （CFR） were measured and recorded. Cardiac output （CO） （AFR ＋ CFR） and hydraulic work （CO × MAP/wet heart weight） were calculated. After 10 min epuilibration period, normal saline （NS） or different amount of propofol was added to perfusate [0 （blank control n = 6）, 0.1 （n = 5）, 1.0 （n = 6）, 5.0 （n = 5）, 10.0 （ n = 6） and 50.0 （ n = 5） μmol·L^-1 propofol]. 1 ml of perfusate was taken every 10 min until the end of experiment （80 min） for determination of triacylglycerol （TAG） and lipid oxidation rate. At the end of the experiment the hearts were harvested and frozen for measurement of myocardial lipoprotein lipase activity. In control group the animals were not subjected to myocardial ischemia. Results Significantly less hydraulic work was done in I/R group than in control group when no propofol was added to perfusate （blank control subgroup）.Hydraulic work was decreasing with increasing propofol concentration in control group but in I/R group hydraulic work was increased when propofol was added to perfusate as compared to the blank control subgroup. In both groups perfusate TAG concentration was significantly increased in propofol 5.0, 10.0, 50.0μmol·L^-1 subgroups as compared to blank control subgroup. In I/R group lipid oxidation and myocardial lipoprotein lipase （LPL） activity were significantly decreased in propofol 5.0, 10.0, 50.0μmol·L^-1 subgroup as compared to NS blank control subgroup; whereas in control group there was no significant difference in lipid oxidation and myocardial LPL activity among the 6 subgroups. Conclusion Profofol has protective effect on heart function against I/R by improving myocardial lipid metabolism.
出处
《中华麻醉学杂志》
CAS
CSCD
北大核心
2006年第7期634-637,共4页
Chinese Journal of Anesthesiology
基金
国家自然科学基金资助项目(30170906)
关键词
二异丙酚
心肌再灌注损伤
脂类
Propofol
Myocardial reperfusion injury
Lipids
