期刊文献+

热休克对再灌注性心律失常的影响及其作用机制的研究 被引量:2

Effect and Mechanism of Heat Shock Response on Reperfusion Arrhythmias in Rat
下载PDF
导出
摘要 目的 :研究热休克预处理对 SD大鼠再灌注性心律失常的影响及其作用机制。  方法 :将 32只 SD大鼠随机分为热休克组 (n=16 )和对照组 (n=16 )。热休克组大鼠给予热休克预处理而对照组则否。采用 L angendorff离体心脏灌注法 ,先稳定灌注 40分 ,再停灌 2 0分 ,然后复灌 6 0分。心电图记录再灌注时心律失常情况。并检测再灌注时心脏流出液肌酸激酶 (CK)的活性。以 Western blot法检测两组心脏组织中 70 KD热休克蛋白(HSP70 )的相对含量。另外还检测心肌组织中的超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶 (GSH- Px)和过氧化氢酶(CAT)等抗氧化酶的活性 ,及脂质过氧化物丙二醛 (MDA)的含量。  结果 :热休克组的再灌注性心律失常发生率明显较对照组为低 ,表现为心室颤动发生率在热休克组为 0 ,而对照组为 6 / 16。室性心动过速发生率热休克组为 3/ 16 ,而对照组为 7/ 16 ,以热休克组为低 (P<0 .0 5 )。再灌注过程中心肌 CK的释放量热休克组 31.4± 6 .8IU/ L 较对照组 42 .3± 8.9IU/ L显著减少 (P<0 .0 0 1)。热休克组心脏组织 HSP70表达量较对照组显著增多 ,信号条带积分吸光值热休克组为 6 .39± 1.98,对照组为 4.6 2± 2 .0 5 (P<0 .0 1)。热休克组抗氧化酶活性较对照组明显增强 ,而脂质过氧化物则降? Objective:To investigate the effect and mechanism of heat shock response on reperfusion arrhythmias (RAs) in rat. Methods:Thirty two Sprague Dawley rats were randomly divided into 2 groups:the heat shock group (group H) and the control group (group C).Twenty four hours after heat shock preconditioning,the hearts of rats in group H were excised and mounted on a non circulating Langendorff perfusion apparatus and perfused retrogradely with modified K H buffer.After perfused for a stable period of 40 min,global ischemia was induced for 20 min followed by 60 min reperfusion.The rats in group C were treated similarly as that in group H except that they needn't to be preconditioned with heat shock.RAs were recorded and the effluent during reperfusion was collected for measurement of creatine kinase (CK).Finally the hearts were stored in liquid nitrogen for measurement of heat shock protein(HSP) 70 (by Western bloting),the activity of anti oxydase (SOD,GSH Px,CAT) and lipid peroxydative products MDA. Results:Prior heat stress significantly decreased reperfusion arrhythmias.No ventricular fibrillation (VF) was seen in group H,while the incidence of VF in group C was 6/16.The incidence of ventricular tachycardia (VT) in group H was 3/16 while 7/16 in group C( p <0 05).The amount of CK release in the effluent in group H was much less than that in group C(31 4±6 8 IU/L vs.42 3±8 9 IU/L, p <0 001).Myocardial HSP70 content was elevated significantly in group H.Optical density ratios of group H and C were 6.39±1.98 vs.4.62±2.05 ( p <0.01).Additionally,heat stress significantly increased myocardial anti oxydases activity and decreased lipid peroxydative products. Conclusion:Heat shock pretreatment markedly reduces ischemia/reperfusion induced injury of heart and ventricular arrhythmias in rat and this effect is associated with the increase of myocardial HSP70 and activity of anti oxydase activity.
出处 《中国循环杂志》 CSCD 北大核心 2001年第1期21-23,共3页 Chinese Circulation Journal
基金 国家自然科学基金!资助项目 (39570 31 6)
关键词 Langendorff灌流模型 心律失常 热休克蛋白类 Langendorff perfusion model Arrhythmia Heat shock proteins Rat
  • 相关文献

参考文献11

  • 1[1]Walker MJA,Curtis MJ,Hearse DJ,et al.The Lambeth Conventions:guidelines for the study of arrhythmia in ischemia,infarction,and reperfusion.Cardiovasc Res,1988,22:447—455.
  • 2[2]Curtis MJ,Walker MJA.Quantification of arrhythmias using scoring systems:an examination of seven scores in an in vivo model of regional myocardial ischemia.Cardiovasc Res,1988,22:656—665.
  • 3[3]Donnelly TJ,Sievers RE,Vissern FLJ,et al.Heat shock protein induction in rat heart:a role for improved myocardial salvage after ischemia reperfusion?Circulation,1992,85:769—778.
  • 4[4]Marber MS,Latchman DS,Walker JM,et al.Cardiac stress protein elevation 24 hours after brief ischemia or heat stress is associated with resistance to myocardial infarction.Circulation,1993,88:1264—1272.
  • 5[5]Currie RW,Karmazyn M,Kloc M,et al.Heat shock response is associated with enhanced postischemic ventricular recovery.Circ Res,1988,63:543—549.
  • 6[6]Steare SE,Yellon DM.The protective effect of heat stress against reperfusion arrhythmia in the rat.J Mol Cell Cardiol,1993,25:1471—1481.
  • 7[7]Georgopoulos C,Welch WJ.Role of the major heat shock proteins as molecular chaperones.Annu Rev Cell Biol,1993,9:601—634.
  • 8[8]Kampinga HH.Thermotolerance in mammalian cells.Protein denaturation and aggregation,and stress proteins.J Cell Sci,1993,104:11—17.
  • 9[9]Barrington PL,Meier CF Jr,Weglicki WB.Abnormal electrical activity induced by free radical generating system in isolated cardiomyocytes.J Mol Cell Cardiol,1988,20:1163—1178.
  • 10[10]Yoshida T,Maulik N,Engelman RM,et al.Glutathione peroxidase knockout mice are susceptible to myocardial ischemia reperfusion injury.Circulation,1997,96(Suppl Ⅱ):Ⅱ216—220.

同被引文献72

  • 1[46]Qian YZ, Shipley JB, Levasseur JE, et al. Dissociation of heat shock proteins expression with ischemic tolerance by whole body hyperthermia in rat heart.J Mol Cell Cardiol,1998,30(6):1163-1172.
  • 2[47]Qian YZ, Bernardo NL,Nayeem MA,et al.Induction of 72-kDa heat shock protein does not produce second window of ischemic preconditioning in rat heart. Am J Physiol, 1999,276(1 Pt 2): H224-234.
  • 3[48]Heads RJ, Baxter GF, Latchman DS, et al. Hsp and cytoskeletal protein expression and localization during delayed preconditioning in the rabbit heart. J Mol Cell Cardiol,1998,30(suppl):A20.
  • 4[49]Dana A, Skarli M, Papakrivopoulou J, et al. Adenosine A(1) receptor induced delayed preconditioning in rabbits: induction of p38 mitogen-activated protein kinase activation and Hsp27 phosphorylation via a tyrosine kinase- and protein kinase C-dependent mechanism.Circ Res,2000,86(9):989-997.
  • 5[50]Baxter GF, Goma FM, Yellon DM. Involvement of protein kinase C in the delayed cytoprotection following sublethal ischaemia in rabbit myocardium.Br J Pharmacol,1995,115(2):222-224.
  • 6[51]Liu H, McPherson BC, Yao Z. Preconditioning attenuates apoptosis and necrosis: role of protein kinase C epsilon and -delta isoforms. Am J Physiol Heart Circ Physiol,2001,281(1):H404-410.
  • 7[52]Imagawa J, Baxter GF, Yellon DM, et al. Genistein, a tyrosine kinase inhibitor, blocks the "second window of protection" 48 h after ischemic preconditioning in the rabbit.J Mol Cell Cardiol,1997,29(7):1885-1893.
  • 8[53]Dawn B, Xuan YT, Qiu Y, et al. Bifunctional role of protein tyrosine kinases in late preconditioning against myocardial stunning in conscious rabbits.Circ Res, 1999,85(12):1154-1163,998-1004.
  • 9[1]Murry CE, Jennings RB, Reimer KA. Preconditioning with ischemia:a delay of lethal cell injury in ischemic myocardium.Circulation,1986,74(5):1124-1136.
  • 10[2]Bolli R.The early and late phases of preconditioning against myocardial stunning and the essential role of oxyradicals in the late phase: an overview. Basic Res Cardiol,1996,91(1):57-63.

引证文献2

二级引证文献6

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部