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缺血预处理对心肌组织酶的活性影响实验研究 被引量:1

Effect of Ischemic Preconditioning on Activities of Phospholipase A2 and ATPase of Myocardial Cells during Cardiopulmonary Bypass
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摘要 目的 观察缺血预处理 (IPC)对体外循环 (CPB)中缺血再灌注心肌组织磷酯酶A2 (PLA2 )和ATPase活性的影响 ,评价其对心肌的保护作用 ,并初步探讨其可能的作用机制。方法 在猫CPB模型的基础上 ,比较IPC组和缺血再灌注组CPB中心肌组织PLA2 及Na+ -K+ -ATPase、Ca2 + -Mg2 + -ATPase、Ca2 + -ATPase活性。结果 IPC处理组可明显减轻CPB中缺血再灌注导致的PLA2 活性升高和ATPase活性下降。结论 IPC可能通过减轻缺血再灌注期间的Ca2 + OBJECTIVE To elucidate the influences of ischemic preconditioning(IPC)on activity of Phospholipase A 2 and ATPase of ischemia / reperfusion myocardial cell during cardiopulmonary bypass(CPB).METHODS Ninety felines were randomized into there groups: GroupⅠ(n=30),in which CPB was conducted without aortic cross-clamping (ACC); Group Ⅱ(n=30),with 60min ACC followed by 90 min reperfusion, and cardioplegia used during period of ACC; Group Ⅲ(n=30), with protocol similar to that of group Ⅱ except for three-round 15 min IPC applied before ACC. Activities of PLA 2 and Na +-K- +ATPase、Ca 2+-Mg 2+-ATPase andCa 2+-ATPase of myocardial cells were simultaneously measured during ACC and reperfusion periods. RESULTS IPC significantly alleviated the upregulation of activity of PLA 2 and the inhibition of activity of Na +-K- +ATPase、Ca 2+-Mg 2+-ATPase and Ca 2+-ATPase of myocardium during periods of ischemia and reperfusion. CONCLUSION IPC can protect myocardial cells from ischemia and reperfusion injury during CPB by regulating the activities of PLA 2 and the ATPases of myocardium, which may alleviate of Ca 2+overload and hydrolysis of membrane phospholipid.
出处 《中国体外循环杂志》 2003年第3期167-169,共3页 Chinese Journal of Extracorporeal Circulation
基金 上海市科技启明星项目 曙光计划资助项目
关键词 缺血预处理 心肌缺血 体外循环 再灌注损伤 磷酯酶A2活性 ATPASE活性 心肌保护 cardiopulmonary bypass myocardial reperfusion injury phospholipase ATPase ischemic preconditioning.
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  • 1陈晓东,王志农,张宝仁,朱家麟,蔡凯华,丁芳宝.体外循环中心肌缺血再灌注损伤与恢复的超微结构研究[J].第二军医大学学报,1997,18(S1):82-85. 被引量:17
  • 2[3]Martin HB,Walter CL.Preconditioning:an endogenous defense against the insult of myocardial ischemia[J].Anesth Analg,1996,83(3):639-645.
  • 3[4]Fliss H,Gattinger D.Apoptosis in ischemic and reperfused rat myocardium[J].Circ Res,1996,79(5):949-956.
  • 4[5]Javadov S,Karmazyn M.Mitechondrial permeability transition pore opening as an endpoint to initiate cell death and as putarive target for cardioprotection[J].Cell Physiol Biochem,2007,20(1-4):1-22.
  • 5[7]Bevers EM,Comfurius P,Dekkers DW,et al.Regulatory mechanisms of transmembrane phospholipid distributions and pathophysiological implications of transbilayer lipid scrambling[J].Lupus,1998,7(supp12):s126-131.
  • 6[8]Richter C.Pro-oxidants and mitochondrial Ca2+:their relationship to apoptosis and oncogenesis[J].FEBS,1993,325(1-2):104-107.
  • 7[9]Fabisiak JP,Kagan VE,Ritov VB,et al.Bcl-2 inhibits Betective oxidation and externalization of phosphatidylsefine during paraquat-induced apoptosis[J].Am J Physiol,1997,272(2Pt 1):C675-684.
  • 8[10]Freude B,Masters TN,Robicsck F,et al.Apoptoeis is initiated by myocardial ischemia and executed during reperfusion[J].J Mol Cell Cardiol.2000,32:197-208.
  • 9[11]Grover GJ,Garlid KD.ATP-Sensitive potassium channels:A review of their cardioprotective pharmacology[J].J Mol Cell Cardiol,2000,32(4):677-695.
  • 10曾志勇,王志农,何斌,徐志云,张宝仁.猫体外循环时心肌caspase3 mRNA表达的变化[J].第二军医大学学报,2004,25(4):383-385. 被引量:8

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