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超极化停搏对体外循环中心肌组织磷酯酶A2及ATPase活性的影响 被引量:1

Effect of hyperpolarized arrest on activities of phospholipase A_2 and ATPase of myocardial cells during cardiopulmonary bypass
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摘要 目的观察超极化停搏(超极化停搏)对体外循环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。方法在猫体外循环模型的基础上,比较超极化停搏组和去极化停搏组体外循环中心肌组织PLA2及Na+-K+-ATPase、Ca2+-Mg2+-ATPase和Ca2+-ATPase活性。结果超极化停搏处理组可明显减轻体外循环中缺血再灌注导致的PLA2活性升高和ATPase活性下降。结论超极化停搏可能通过减轻缺血再灌注期间的Ca2+超载及抑制细胞膜磷脂水解而发挥其心肌保护作用。 [Objective] To elucidate the influences of hyperpolarized arrest on activity of phospholipase A2 and ATPase of ischemia/repeffusion myocardial cell during cardiopulmonary bypass(CPB). [Methods] Seventy-five felines were randomized into three groups: simply CPB group, depolarized arrest group and hyperpolarized arrest group. In simple CPB group, CPB was conducted without aortic cross-clamping (ACC). In depolarized arrest group and hyperpolarized arrest group, hearts underwent 60 minutes of global ischemia after ACC and infusion of cardioplegic solution (10 mL/kg), followed by 90 minutes of repeffusion. The cardioplegic solution consisted of St. Thomas solution with KCl (16 mmol/L) in depolarized arrest group or pinacidil (50 mmol/L) in hyperpolarized arrest group. Activities of PLA2 and Na^+-K-^+ATPase, Ca^2+-Mg^2+ ATPase and Ca^2+-ATPase of myocardial cells were simultaneously measured during ACC and reperfusion periods. [Results] Hyperpolarized arrest significantly alleviated the upregulated activity of PLA2 and the inhibited activities of Na+-K-^+ATPase, Ca^2+-Mg^2+-ATPase and Ca^2+-ATPase of myocardium during periods of ischemia and repeffusion. [Conlusion] Hyperpolarized arrest can protect myocardial cells from ischemia and reperfusion injury during CPB by regulating the activities of PLA2 and the ATPases of myocardium, which may duo to alleviation of Ca^2+ overload and hydrolysis of membrane phospholipid.
出处 《中国现代医学杂志》 CAS CSCD 北大核心 2007年第21期2589-2592,共4页 China Journal of Modern Medicine
基金 福建省自然科学基金资助项目(C0110026)
关键词 体外循环 心肌再灌注损伤 磷酯酶 ATP酶 超极化停搏 cardiopulmonary bypass myocardial reperfusion injury phospholipase ATPase hyperpolarized arrest
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  • 1ALTAVILLA D, SQUADRITO F, CAMPO GM, et al. The reduction of myocardial damage and leukocyte polymorphonuclear accumulation following coronary artery occlusion by the tyrosine kinase inhibitor tyrphostin AG 556 [J]. Life Sci, 2000, 67:2615-2629.
  • 2CAI Z, MANALO DJ, WEI G, et al. Hearts from rodents exposed to intermittent hypoxia or erythropoietin are protected against ischemia-reperfusion injury[J]. Circulation, 2003, 108(1):79-85.
  • 3SCHULZ R, AKER S, BELOSJOROW S, et al. TNFalpha in ischemia/reperfusion injury and heart failure[J]. Basic Res Cardiol,2004, 99(1): 8-11.
  • 4GWECHENBERGER M, MENDOZA LH, YOUKER KA,et al.Cardiac myocytes produce interleukin-6 in culture and in viable border zone of reperfused infarctions[J]. Circulation, 1999, 99:546-551.
  • 5FRANGOGIANNIS NG, LINDSEY LM, MICHAEL LH, et al. Resident cardiac mast cells degranulate and release preformed TNF-α,initiating the cytokine cascade in experimental canine myocardial ischemia/reperfusion[J]. Circulation, 1998, 98: 699-710.
  • 6CALABRESI L, ROSSONI G, GOMARASCHI M, et al.High-density lipoproteins protect isolated rat hearts from ischemia-reperfusion injury by reducing cardiac tumor necrosis factor-alpha content and enhancing prostaglandin release[J]. Circ Res, 2003, 92(3): 330-337.
  • 7BELOJOOROW S, SCHULZ R, DRGE H, et al. Endotoxin and ischemic preconditioning: TNF-α concentration and myocardial infarct development in rabbits[J]. Am J Physiol, 1999, 277(6 pt2): H2470-2475.
  • 8ERIKSON JM, FREEMAN GL, CHANDRASEKAR B. Ultrasound-targeted antisense oligonucleotide attenuates ischemia/reperfusion-induced myocardial tumor necrosis factor-alpha[J]. J Mol Cell Cardiol, 2003, 35(1): 119-130.
  • 9YOKOYAMA T, VACA L, ROSSEN RD, et al. Cellular basis for the negative inotropic effects of tumor necrosis factor-alpha in the adult mammalian heart [J]. J Clin Invest, 1993, 92:2303-2312.
  • 10SMITH RM, SULEMAN N, MCCARTHY J, et al. Classic ischemic but not pharmacologic preconditioning is abrogated following genetic ablation of the TNFalpha gene[J]. Cardiovasc Res,2002, 55(3): 553-560.

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  • 1林思芳,杨光,周青山,黄海波.缺血预处理对再灌注心肌肿瘤坏死因子-α、白介素-6的影响[J].中国现代医学杂志,2005,15(13):1958-1961. 被引量:5
  • 2Hoffman JW Jr, Gilbert TB, Poston RS, et al. Myocardial reperfusion injury: etiology, mechanisms, and therapies[ J]. J Extra Corpor Technol,2004,36 ( 4 ) : 391-411.
  • 3Kaneko M, Matsumoto Y, Hayashi H, et al. Oxygen free radicals and calcium homeostasis in the heart [ J ]. Mol Cell Biochem, 1994, 139(1) :91-100.
  • 4Weiss JN, Korge P, Honda HM, et al. Role of the mitochondrial permeability transition in myocardial disease [ J ]. Circ Res, 2003,93 (4) :292-301.
  • 5Chen YF, Lin YT. Comparison of blood cardioplegia to electrolyte cardioplegia on the effectiveness of preservation of right atrial myo- cardium : mitochondrial morphometric study [ J ]. Ann Thorac Surg, 1985,39(2) :134-138.
  • 6Prodinser WM, Wurzner R, Erdei A, et al. Complement In: Patti WE, ed. Fundamental immunology [ M ]. Philadelphia: LippincottRaven, 1999:967-985.
  • 7Toyoda Y, Yamaguchi M, Yoshimura N, et al. Cardioproteetive effects and the mechanisms of terminal warm blood cardioplegia in pediatric cardiac surgery [ J ]. J Thorac Cardiovasc Surg, 2003,125 (6) :1242-1251.
  • 8刘和俊,汪太平,李芹,史学功.急性心肌梗死患者氧化损伤及抗氧化酶活性[J].中国动脉硬化杂志,2001,9(4):319-321. 被引量:13

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