复方中药制剂对运动大鼠心肌的保护作用及机制研究
详细信息    本馆镜像全文|  推荐本文 |  |   获取CNKI官网全文
摘要
1研究目的
     通过让大鼠服用中药复方制剂,比较各组大鼠在不同状态下心肌组织各生化指标的差异,探讨了运动导致心肌损伤的机理及游泳训练、中药复方制剂在保护大鼠心肌组织氧化应激损伤中起到的作用。为更好的指导运动训练、促进运动疲劳的恢复、及为复方中药制剂的开发提供理论支持。
     2研究方法
     8周龄雌性Wistar大鼠140只,体重约200g,随机分为4组:A(安静组)、B(服药组)、C(运动训练组)、D(运动训练+服药组)。A、C组正常进食和饮用凉开水,B、D组以用复方中药制剂代替凉开水饮用。C、D组持续8周游泳训练,尾部负自身体重3%的重物,第1周训练时间为30min,之后每周递增10min;第8周增为100min:8周后每个组再分安静、力竭即刻、定量运动1h、力竭恢复12h、力竭恢复24h 5个亚组,于相应时刻断头处死;取心肌待测MDA、总Ca~(2+)、LD含量及LHD、SOD、Ca~(2+)-ATPase、Na~+-K~+-ATPase活性。所有数据用SPSS12.0统计软件进行T检验,显著水平为p<0.05。
     3实验结果
     3.1安静状态
     MDA含量训练+服药组显著低于其它3组(P<0.05),服药组显著低于安静组(P<0.01);SOD活性训练+服药组活性显著高于其它3组(P<0.01),服药组和训练组显著高于安静组(P<0.05),Ca~(2+)-ATPase的活性,训练+服药组显著高于安静组和服药组(P<0.05),服药组显著高于安静组P<0.05。
     3.2力竭后即刻
     MDA含量安静组显著高于其它3组(P<0.01);SOD活性,训练+服药组显著高于其它3组(P<0.01),服药组和训练组均显著高于安静组;总Ca~(2+)含量,安静组显著高于其它3组,(P<0.01),训练+服药组显著低于服药组和训练组(P<0.01);Ca~(2+)-ATPase活性,训练+服药组显著高于其它3组(P<0.05),服药组显著高于安静组(P<0.05);LD含量,训练+服药组显著低于安静组(P<0.05);LDH活性训练+服药组显著性高于安静组和运动训练组(P<0.05),同时还极显著高于服药组(P<0.01)。
     3.3定量运动1小时
     MDA含量训练+服药组非常显著安静组(P<0.01),训练+服药组还显著低于训练组(P<0.05);SOD活性训练+服药组显著性高于安静组和服药组(P<0.01),训练+服药组SOD活性也显著性高于训练组(P<0.05),服药组显著性高于安静组(P<0.01);训练组显著性高于安静组P(<0.05);总Ca~(2+)含量,服药组和训练+服药组显著低于安静组(P<0.01),训练+服药组总Ca~(2+)含量也显著低于服药组(P<0.05),训练+服药组也非常显著低于训练组(P<0.01);Ca~(2+)-ATPase活性,各组都显著高于安静组(P<0.05),训练+服药组也显著高于训练组(P<0.05);Na~+-K~+-ATPase、LD、LDH各指标各组之间并无显著性差异(P>0.05)。
     3.4力竭后恢复12小时
     MDA含量训练+服药组显著性低于安静组P(<0.05);SOD活性服药组和训练+服药组两组显著高于安静组(P<0.05);训练组显著高于安静组(P<0.05),训练+服药还显著性高于服药组和训练组(P<0.05);总Ca~(2+)含量,服药组显著低于安静组(P<0.01),训练组显著低于安静组(P<0.05),训练+服药组显著低于其它各组(P<0.01);Ca~(2+)-ATPase活性,服药组和训练+服药组均显著高于安静组(P<0.01),训练+服药组活性显著高于训练组(P<0.05);Na~+-K~+-ATPase活性训练+服药组也显著高于服药组和训练组(P<0.01),训练+服药组显著高于安静组(P<0.05);LD含量训练+服药组显著低于安静组(P<0.05),训练+服药组也显著低于训练组P<0.01;安静组LDH活性极显著性低于其它各组(P<0.01),而其它各组之间未出现显著性差异(P>0.05)。
     3.5力竭后恢复24小时
     MDA含量训练+服药组显著低于安静组(P<0.01);SOD活性各组均显著高于安静组(P<0.01),训练+服药组也显著高于服药组(P<0.01),训练+服药组还显著高于训练组(P<0.05);总Ca~(2+)含量各组均显著高于安静组(P<0.01),训练+服药组还显著高于服药组和训练组(P<0.01);Ca~(2+)-ATPase活性训练+服药组活性显著高于安静组和训练组(P<0.01),服药组显著高于安静组(P<0.01);Na~+-K~+-ATPase活性训练+服药组显著高于安静组和服药组(P<0.05),训练+服药组活性还显著高于训练组P<0.01;LD和LDH在各组之间未出现显著性差异(P>0.05)。
     4结论
     4.1 8周游泳训练可能通过运动预适应机制提高大鼠心肌组织抗氧化能力,减少脂质过氧化反应;对维持心肌细胞内环境稳定性,保持大鼠心肌细胞膜完整性,保护心肌组织起到了积极的作用。
     4.2复方中药制剂在主动清除大鼠心肌内自由基,减少脂质过氧化反应,提高大鼠心肌组织抗氧化能力;维持心肌细胞内环境的稳定性,有效抑制心肌细胞内钙超载的发生,保护细胞的完整性起到积极作用。
     4.3有氧耐力训练与复方中药制剂的联合使用对于保护大鼠心肌免于氧化应激损伤及促进损伤后的恢复都起到了更为积极的作用,比单纯使用一种方法的效果更为明显。
1 Objective:
     The main purpose of this paper is to observe the influence of the compound prescription of Chinese traditional antioxidial medicne on the enzyme activity or some contnet of the rats cardium and serum from different group rats,discuss the merchanism of the cardium antioxidial injury and how can the medicine to protect the cardium from injuring.In order to provide some scientific theory basis of training and explore some chinese medicine bavery for protecting the cardium from injuring.
     2 Method:
     120 female Wister rats were randomly selected and divieded into 4 groups:A(the peachful control group),B(the peathful group to fill medicine group),C(movement training group),D(movement training plus medicine group).The A,C group drink water freely every day,while the B,D group drink the chinese medicine bavery institute water.And,the C,D group LDst 8 weeks swimming train with a load about 3%of their own body on the tile:at the first week,the training time is 30 minutes every day;the second week,is 40 minutes...;like this the training time is 10 minutes more than the before week.So the training time is 100 minutes at the 8th week every day.After 8 weeks,divid each group into 5 subnits stochastically:the peachful group,the quota load 1 hour group,the strength using up group,the 12 hour recovery group after strength using up,the 24 hour recovery group after strength using up.The activity of the SOD、LDH、Ca~(2+)-ATPase、Na~+-K~+-ATPase from cardium and the MDA、total Ca~(2+)、LD content from cardium were measured.All data count uses the software with SPSS12.0 to carry on the T-test,the obviouse standard is P<0.05,the very obviouse standard is P<0.01.The software with Word 2003 to picture.
     3 Results:
     3.1 In quite stae,in the tissue of cardaic muscle,the MDA content of group C is very obviously lower than group A(P<0.01);group D is higher than the other groups.The activity of SOD in group B and C are both higher than group A(P<0.05);group D is very obviousyly higher than the other groups,P<0.01;the activity of Ca~(2+)-ATPase in group C is higher then group A(P<0.05);group D is higher than group B and C(P<0.05).
     3.2 At the immediate ends of exhaustive exercise,in the tissue of cardaic muscle,the content of MDA in other three groups are very lower than group A obviously,(P<0.01);the activity of SOD in the group B and C are both higher than group A(P<0.05);and group D is very obviously higher than the other three groups,(P<0.01);the content of total Ca~(2+) in the other three groups are very obviously lower than group A(P<0.01);and group D is the lowest.the activity of Ca~(2+)-ATPase in group B is obviously higher than group A(P<0.05);and group D is the lowest in the four groups.the content of LD in group D is obviously lower than group A(P<0.05).the activitity of LDH in group D is obviously higher than group A and C(P<0.05),also very obviously higher than group B(P<0.01)..
     3.3 In the quota load 1 hour conditon,in the tissue of cardaic muscle,the content of MDA in group D is lower than group A and B obviously;the activity of SOD in group C is very obviously higher than group A(P<0.01);group B is obviously higher than group A,(P<0.05);also,group D is the highest in the four groups;the cotent of total Ca~(2+) in group B and D is very obviously lower than group A(P<0.01);also,group A is lower than ther other two groups.the activity of Ca~(2+)-ATPase in other three groups are higher than group A,P<0.05,and group D is the highest among the four groups.
     3.4 In the condition of 12 hour recovery after strength using up,in the tissue of cardaic muscle,the content of MDA in group D is obviously lower than group A,P(<0.05 );the activity of SOD in group B and D are both higher than group A,(P<0.05);also,group D is obviously higher than group B and C(P<0.05).the content of total Ca2+ in group B is very obviously lower than group A(P<0.01);group C is obviously lower than group A(P<0.05);and group D is very obviously lower than other three groups;the activity of Ca~(2+)-ATPase in group B and D are both very obviously higher than group A(P<0.01);and group D is obviously higher than group C(P<0.05);the activity of Na~+-K~+-ATPase in group D is obviously higher than group A,P<0.05;however,group D is very obviously higher than group B and C(P<0.01);he content of LD in group D is obviously lower than group A,and very obviously lower than group B.the activity of group A is very obviously lower than the other three groups(P<0.01),but,there is no difference among the three groups..
     3.5 In the condition of 12 hour recovery after strength using up,in the tissue of cardaic muscle,the content of MDA in group D is very obviously lower than group A(P<0.01);the activity in the other three groups are very obviously higher than group A,(P<0.01);group D is also lower than group B and C;the content of total Ca~(2+) in the other three groups are very obviously higher than group A,(P<0.01);and group D is very obviously lower than group B and C(P<0.01);the activity of Ca~(2+)-ATPase in group B is very obviously higher than group A, (P<0.01);group D is very obviously higher than group A and B,P<0.01;the activity of Na~+-K~+-ATPase in group D is obviously higher than both group A and B(P<0.05);also,group D is very obviously higher than group B(P<0.01).
     4 conclusion
     4.1 The 8 weeks cyclical aerobic endurance swimming training may improves rats antioxidant capacity in myocardial tissue,To maintain the integrity of myocardial cell membrane;and play a important role in the progress of protectiing myocardial tissue.
     4.2 The antioxidant compound chinese medicine can clear the free radicals in rat myocardium, reduces lipid peroxidation,improves rat antioxidant capacity in myocardial tissue;there is conducive to the maintenance of myocardial cells within the environment of stability, effectively;so that,it inhibites the occurrence of calcium overload,protects the integrity of the cells;and play a postive in the recovery progress of myocardial injury after exercise.
     4.3 Aerobic endurance swimming training with the compound of the joint use of antioxidant compound chinese medicine is very positively from oxidative stress injury and to promote recovery after injury;of course the jiont use is more effective than simply a method.
引文
[1]Roberto Bolli et al.J Clin Invest,1995,96(8):1066-1084.
    [2]Harsdorf R V,LI P F,DIETZ R.Signaling pathways inreactive oxygen species-induced cardionyocyie apopiosis[J].CircuLDtion,1999,99(22):2934-2941.
    [3]AIKAWE R,NAGAI T,TANAKA M,et al.Reactiveoxygen species in mechanical stree-induced cardiac hypertrophy[J].Biochem Biophys Res Commun,2001,289(4):901-907.
    [4]NI R Z,HUANG J F,XIAO M B,et al.Glycylprolinedipeptidyl aminop eptidase isoenzyme in diagnesis of primaryhepatocelluLDr carcinoma[J].World J Gastroenterol,2003,9(4):710.
    [5]游琪,蔡久英.氧化应激与心肌损伤的研究进展[J].临床荟萃,2005,20(19):1127-1129.
    [6]马彬,景志强,张钧.过度训练对心肌组织影响的研究进展[J].南京体育学院学报(自然科学版),2006,5(1):67-70.
    [7]王文成,刘克敏.力竭运动对小鼠心肌线粒体自由基代谢和线粒体功能的影响[J].广州体育学院学报,2008,28(1):106-108.
    [8]韩长良.力竭性运动对心脏影响作用的研究进展[J].井冈山医专学报,2006,13(4):35-36.
    [9]王沛.过度训练对大鼠血清心肌酶活性的影响[J].西安体育学院学报,2001,18(2):35-37.
    [10]PaoLDVenditti,PieroMasullo,SergioDi Meo,et al.Effects of prolonged aerobic exercise on myocardial responses to ischaemia reperfusion in therat.[J]Experimental Physiology,2001,86(3):341,348.,
    [11]FrankJGiordano.Oxygen,oxidative stress,hypoxia and heart failure[J].Clin.Invest,2005,115:500-508.
    [12]Scott KPowers,John Quindry,Karyn Hamilton.Aging,Exercise,and Car-dioprotection[J].Ann.N.Y.Acad.Sci,2004,1019:462-470.
    [13]]Demirel,Haydar A,Scott K Powers,et al.Short-term exercise improversmyocardial tolerance to in vivo ischemia-reperfusion in the rat[J].J ApplPhysiol,2001,91:2205-2212.
    [14]Lennon,Shannon L,John Quindry,et al.Loss of exercise-induced cardi oprotection after cessation of exercise[J].Jappl Physiol,2004,96:1229-1305.
    [15]S L Lennon,J C Quindry,J P French,et al.Exercise and myocardial tolerance toischaemia-reperfusion[J].Acta Physiologica Scandi -navica,2004,182(2):161-169.
    [16]Hyosook Hwang,Peter J Reiser,George E.Billman Effects of exercisetraining on contractile function in myocardial trabecuLDe after ischemia-reperfusion[J].J Appl Physiol,2005,99:230-236.
    [17]Joseph R Libonati,Zebulon VKendrick,Steven R Houser.Sprint trainingimproves postischemic,left ventricuLDr diastolic performance[J].J ApplPhysiol,2005,99:2 121-2 127.
    [18]Diffee GaryM,Eric ASeversen,Marci MTitus.Exercise training increases the Ca2+sensitivityof tension in rat cardiac myocytes[J].J Appl Physiol,2001,91:309-315.
    [19]Palmer Bradley M,Eric A Mokelke,Anne M.Thayer,et al.Mild renal hyper -tension alters run training effects on the frequency response of ratcardiomyocyte mechanics[J].J Appl Physiol,2003,95:1 799-1 807.
    [20]Frances MAshcroft.ATP-sensitive potassiumchannelopathies:focus on -insulin secretion[J].J.Clin.Invest,2005,115:2 047-2 058.
    [21]Yigang Wang,En Takashi,Meifeng Xu,et al.DownreguLDtion of ProteinKinase C Inhibits Activation of Mitochondrial KATP Channels by Dia-zoxide[J].CircuLDtion,2001,104:85-90.
    [22]David A Brown,Adam J Chicco,Korinne N Jew,et al.Cardioprotection afforded by chronic exercise is mediated by the sarcolemmal,and notthe mitochondrial,isoform of the KATP channel in the rat[J].J Phy siol,2005,569:913-924.
    [23]David A.Brown,Joshua M.Lynch,CaseyJ.Armstrong,et al.Susceptibility of the heart to ischaemia-reperfusion injury and exercise-induced car-dioprotection are sex-dependent in the rat[J].J Physiol,2005,564(Pt 2):619-630.
    [24]翟庆峰.运动预适应对心肌相对缺血/再灌注损伤的延迟保护作用及机制研究.中国人民解放军军事医学科学学院[D],硕士毕业论文,2005.
    [25]彭峰林,陈建文,任琦等.间歇运动训练对心脏缺血再灌注损伤大鼠心肌抗化酶的影响[J].中国运动医学杂志,2008,27(1):97-99.
    [26]田振军,熊正英,郭进,等.大鼠游泳过度训练模型的建立及心室构型改建研究[J]。陕西师范大学学报(自然科学版),1996,24(3):104-109.
    [27]隋波,康健,张虞毅,等耐力运动对自由基、血清超氧化物歧化酶活性影响的研究[J].山东体育学院学报,2001,17(3):31-33.
    [28]Venditi P,DiMeo S.Effect of training on antioxidant capacity tissue damage,endendrance of adult male rats[J],Int Sports Med,1997,18(7):497-502.
    [29]郭林,平永忠,曹建民,等.耐久性运动导致大鼠肾脏组织自由基代谢动态变化的研究中国体育科技,2001,37(2):8-10.
    [30]郭海英,许豪文.耐力训练对大鼠肝脏、股四头肌中谷耽甘肤含量的影响[J].浙江体育科学,1996,18(5):46-50.
    [31]卢健,赖荣兴,陈彩珍,等.绿茶提取物对运动小鼠心肝骨骼肌抗氧化的影响广州体育 学院学报,1998,18(4):39-42.
    [32]史亚丽,任杰,许豪文.运动训练对小白鼠心肌、肝脏与股四头肌自由基代谢的影响[J]。山东体育学院学报,1994,10(3):16-20.
    [33]V Margonato,G MiLDno,S Allibardi,et al.Swim Training Improves My-ocardial Resistance to Ischemia in Rats[J].Int J Sports Med,2000,21:163-167.
    [34]Hamilton K L,Staib J L,Phillips T,et al.Exercise,antioxidants,andHSP72:protection against myocardial ischemia/reperfusion[J].Free RadicBiol Med,2003,34(7):800- 809.
    [35]史亚丽,辛晓林,王昌留.不同负荷游泳训练及补硒对衰老大鼠心肌抗氧化能力及血清GOT的影响[J].北京体育大学学报,2002,25(5):636-637.
    [36]刘古锋,吴伟康,段新芬,赵迟,唐娟.附子多糖对力竭运动小鼠心肌氧化应激损伤的保护作用[J].海南医学,2008,19(7):67-69.
    [37]唐量,熊正英.葛根总黄酮保护小鼠运动性心肌损伤的实验研究[J].体育科学,200525(3):62-64.
    [38]徐芝芳,郭层城,曾锡银.蒙古黄芪中药对提高持续运动大鼠心肌组织抗自由基能力的研究[J].体育科学,2005,25(2):76-78.
    [39]刘小杰,何国庆,熊正英.沙棘油对小鼠心肌自由基代谢和超微结构的影响[J].营养学报,2002,24(2):26-29.
    [40]张萌,曹新伟,陈士林.粉防己碱的抗氧化能力与心肌保护作用的相关性研究[J].世界科学技术-中医药现代化.2008,10(3):21-26.
    [41]张飞鹏,曾明,李正恩,杜舒书.松针提取液对小鼠心肌、肝脏、股四头肌自由基代谢的影响[J].山东体育科技,2005,27(3):36-38.
    [42]常英姿,梁殿权,王孝铭,等.丹参素对氧自由基所致大鼠心肌线粒体H+-ATP酶损伤的保护作用[J].中国病理生理学杂志,1991,1(5):449.
    [43]杨卫东,朱鸿良.丹参的氧自由基清除作用[J].中国药理学通报,1990,6(2):118-120.
    [44]Thomas DP,Marshall KI.Effects of repeated exhaustive exercise on myocardial subcellular membrane structures.Int JSports Med,1988,9(4):257-260.
    [45]赵国胜,杨会杰.川芎嗪和丹参对大鼠心脏氧反常保护作用的比较[J].天津医药,1996,24(5):289.
    [45]Bagchi D,et al.[J].Mut Res,2003,523-524:87-97.
    [46]戴友平,唐国华,郭衍坤等.何首乌提取液对犬心肌缺血再灌注损伤的预防作用实验研究[J].中国生化药物杂志,1998,19(2):79-81.
    [47]金哲雄,金政.何首乌对缺氧培养心肌细胞保护作用的实验研究[J].时珍国医国药,2006,17(8):1454-1456.
    [48]王怡,王少霞,仁明,等.首乌参方预处理对大鼠心肌缺血再灌注损伤PKC与iNOsmRNA 表达的影响[J].上海中医药杂志,2007,4(10):75-78.
    [49]刘军,熊正英.Ebselen对大强度耐力训练大鼠心肌自由基代谢和超微结构影响的实验研究西安体育学院学报,2007,24(2):83-85.
    [50]FinaudJ,LDcG.FiLDireE·Oxidativestress:reLDtionshipwithexerciseandtraining[J]·Sports Med,2006,36(4):327-358.
    [51]黄志全.健身跑对中老年人红细胞超氧化物吱化酶活性和血清过氧化酶活性的影响的研究.中国运动医学杂志,1990;9(2):83
    [52]曹国华.运动、锌铜营养与自由基代谢Ⅲ:游泳训练对小鼠体内自由基生成与清除的影响[J].中国运动医学杂志,1991,10(2):65.
    [53]陈月.高水温条件下70分钟游泳运动对小鼠自由基代谢影响的研究[J].南京体育学院学报,1998,12(1):18.
    [54]刘丽萍,柴戬臣,容仕霖,等.游泳训练对大鼠心、肝、肾组织和血清中自由基代谢、CK 和LDH活性的影响[J].体育科学,1999,19(1):80-81.
    [55]金花,许豪文.耐力训练对大鼠大脑、小脑、心肌抗氧化酶及脂褐素含量的影响[J].中国运动医学杂志,1995,14(3):166-169
    [56]Kanter MM,Hamlin RL,Unverferth DV,et al.Effect of exercise training on antioxidant enzymes and cardiotoxicity of doxorubicin.J Appl Physiol 1985,59(4):128-130.
    [57]王效良,黄显忠,王新军等.耐力训练大鼠心肌组织抗氧化指标和超微结构变化与葛根总黄酮的干预[J].中国组织工程研究与临床康复,2007,11(38):23.
    [58]步斌,沈异,雷鸣鸣,孙君志.运动负荷与沙棘对大鼠心肌VEGF表达影响的研究[J].成都体育学院学报,2004,30(6):76-79.
    [59]张清清,施雪药.中药对离体心脏保存与心肌保护的研究进展[J]中药新药与临床药理,2003,14(2):137-139.
    [60]王福文,胡志力,李杰.力竭性运动致运动性心肌损伤的产生机制[J].中国临床康复,2005,28(02).144-46.
    [61]李宏伟,王保平.运动预适应与心肌细胞的保护[J].中国组织工程研究与临床康复,2008,12(24):4740-4744.
    [62]PaoLD Venditti,PieroMasullo,SergioDi Meo,et al.Effects of prolonged aer- obic exercise on myocardial responses to ischaemia reperfusion in the rat.Experimental Physiology,2001,86(3):341,348.
    [63]Scott KPowers,John Quindry,Karyn,Hamilton.Aging,Exercise,and Car-dioprotection[J].Ann.N.Y.Acad.Sci,2004,1 019:462- 470.
    [64]龙碧波,张新定,苏家文.绞股蓝对训练小鼠肝组织自由基代谢及血清酶活性的影响[J].海南师范大学学报(自然科学版)2008,21(2):193-196.
    [65]徐涛,马柯.参附注射液对大鼠心肌损伤的保护作用[J].宁夏医学院学 报,2008,30(6):709-710.
    [66]马先英,孔喜良,黄茂生药对运动大鼠心肌自由基损伤的研究[J]。中国体育科技,2007,43(5):132-135.
    [67]王福文,胡志力,李杰.力竭性运动致运动性心肌损伤的产生机制[J]。中国临床康复,2005,28(02).144-46.
    [68]徐芝芳.蒙古黄芪水煎剂对提高运动大鼠心肌组织抗自由基能力的研究[D]。硕士毕业论文.2003.
    [69]田野.运动生理学高级教程[M].北京:高等教育出版社.2003,8,240-241。
    [70]SculleyJGetal.HumGenet,1992,90:195-207.
    [71]VeLDCetal.MutRes,1998,398:83 -92.
    [72]RobertHHetal.EnvironMolMutagen,1996,28:5-12.[Y]PhillipsEetal.RadiatRes,1995,143:215-262.
    [73]宾晓农,冯炜权,力竭性运动对小鼠心、肾组织MDA与SOD活性的影响[J]。衡阳医学院学报,1995,23(4):244-246.
    [74]王文信,丁树哲,许豪文.长时间游泳运动对大鼠心肌线粒体功能的影响[J]。生物化学和生物物理学报,1991,23(4):243-245.
    [75]祝曦东.复方补气益肾中药对运动大鼠心肌SDH、MDH、LDH、ATP酶的影响[d].硕士学位论文,2008.
    [76]NIRZ,HUANGJF,XIAOMB,etal.GlycylprolinedipeptidyLDminopeptidaseisoenzymeindiagn esisofprimaryhepatocelluLDrcarcinoma[J].WorLDJGastroenterol,2003,9(4):71.
    [77]Masereel B,pochet L,LDeckmann D.An overview of inhibitors of H+/Na+ exchanger.Eormed chem 2003;38:547-554
    [78]AukiranM,Marber MS.H+/Na+ exchanger inhibitors for cardio prote ct ive:therapy,progress,problems and prospects.J Am coll cardiol 2002,39:347-353.
    [79]Schater C,LDdior Y,Inserte J.et al.Role of reverse mode of the Na~+ /Ca~(2+) exchanger in reoxygenation-induced cardiomyocytein jury.Car-diovasres 2001;51:241-250
    [80]张端莲,王瑞绵,周乾毅,程化奇.更年平调液对更年期大鼠心肌保护作用的组织化学研究[J].新中医1997,29(5):35-36.
    [81]庞辉,陈维平,李倩茗,冷静,吕小川.螺旋藻对运动大鼠心肌组织化学影响的研究[J].广西医学,1997,19(4):563-564.
    [82]岳春林,张宗豪。蒙古黄茂对持续运动大鼠糖代谢的影响[J].苏州大学学报,2006,22(2):86-88.
    [83]宋学立,钱令嘉,氧化应激和心肌损伤[J].国外医学卫生学分册,2000,27(1):30-33.
    [84]刘霞.茶多酚对力竭运动小鼠心肌组织钙含量的影响[d].硕士学位论文,2006。

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700