缺血后处理和腺苷后处理对热缺血死亡大鼠供体心脏保护的研究
|
摘要
背景:随着移植技术的发展,供体的缺乏就成为研究人员所面临的一个全球性难题。因此有研究人员开始将研究目光转向无心跳供体/尸体供体(non-heart-beating donors,MHBD),尝试使用临床死亡后的尸体停搏心脏(cadaver non-beating heart,CNBH)来进行心脏移植,以扩大供体的来源。目前研究认为临床有望开发利用的是院外急性失血性休克死亡的CNBH。由于在心脏停搏之前无法进行有效的预处理,因此只能期望在热缺血过程之后通过后处理的方法来减轻心脏因热缺血以及缺血/再灌注所带来的损伤、改善移植后供心的功能。
目的:本研究在首先建立大鼠颈部异位心脏移植模型的基础上,尝试对热缺血死亡后大鼠不同时段的供心,进行缺血后处理以及腺苷后处理,检测受体术后24小时移植心脏的相关指标,来评价其心脏保护作用并探讨可能机制。
方法:实验分为三大部分:
第一部分为大鼠颈部异位心脏移植模型的建立。
第二部分为缺血后处理对热缺血死亡大鼠供体心脏保护的研究。大鼠被随机分为7组:C组—对照组;I_5组、I_(15)组、I_(30)组—单纯热缺血组,供体大鼠失血性休克死亡后单纯热缺血5min、15min、30min取心移植组;P_5组、P_(15)组、P_(30)组—缺血后处理组,供体大鼠失血性休克死亡后热缺血5min、15min、30min取心移植并进行缺血后处理组。移植术后24小时取移植心脏标本,观察其病理改变,检测心甲橹疉TP、SOD、MDA、NF-κB mRNA、TNF-α、IL-6的含量,以及心肌细胞凋亡和Bcl-2、Bax蛋白的表达情况。
第三部分为腺苷后处理对热缺血死亡大鼠供体心脏保护的研究。大鼠被随机分为7组:C组—对照组;I_5组、I_(15)组、I_(30)组—单纯热缺血组,供体大鼠失血性休克死亡后单纯热缺血5min、15min、30min取心移植组;A_5组、A_(15)组、A_(30)组—腺苷后处理组,供体大鼠失血性休克死亡后热缺血5min、15min、30min取心移植并进行腺苷后处理组。移植术后24小时取移植心脏标本,观察其病理改变,检测心肌组织ATP、SOD、MDA、NF-κB mRNA、TNF-α、IL-6的含量,以及心肌细胞凋亡和Bcl-2、Bax蛋白的表达情况。
结果:
1、热缺血死亡30分钟以内,冷缺血1小时左右的大鼠CNBH可以被成功移植。
2、随着热缺血时间的延长,移植心脏的缺血/再灌注损伤越重,病理损害也越重;而在同一时间点与单纯热缺血组相比,缺血后处理组和腺苷后处理组心肌细胞损害被减轻。
3、在同一时间点,缺血后处理以及腺苷后处理与单纯热缺血组相比,可以增加心肌组织的ATP、SOD含量,减少其MDA含量;减少心肌组织的NF-κB mRNA的表达及TNF-α、IL-6的含量;减轻心肌细胞的凋亡水平、上调Bcl-2蛋白表达而下调Bax蛋白表达。
结论:
1、热缺血死亡30分钟以内,冷缺血1小时左右的大鼠CNBH可以被成功应用于心脏移植;
2、缺血后处理以及腺苷后处理对热缺血死亡大鼠心脏移植的供心缺血/再灌注损伤具有保护作用;
3、缺血后处理以及腺苷后处理的心脏保护作用可能与其改善供心的能量代谢、减轻脂质过氧化损伤、抑制NF-κB表达所致炎性损伤以及减少心肌细胞的凋亡有关。
创新点:
1、本实验创新性的将后处理的概念引入心脏移植领域;
2、本实验首次研究缺血后处理对热缺血死亡大鼠供体心脏保护的作用,国内外未见相关报道;
3、本实验首次研究腺苷后处理对热缺血死亡大鼠供体心脏保护的作用,国内外未见相关报道。
不足之处:由于经费、设备等多种限制,无法对移植后的供心进行功能上的检测、相关的检测指标尚不够全面、移植后的观察时间较短。
Background:With the development of transplantation,researchers must face a global problem—the shortage of donors.In order to enlarge the donor pool,some of them turn to non-heart-beating donors(NHBD) and attempt to use cadaver non-beating heart(CNBH)in the heart trans-plantation. Now they think the CNBH received from those who die from acute hemorrhagic shock may be useful.Because none preconditioning methods can be used before the heart stop beating.So we have to try some postconditioning methods to attenuate the warm ischemia and ischemia-reperfusion injury,and to improve the cardiac function after heart transplantation.
Objective:Firstly we try to set up a cervical heterotopic heart trans-plantation in warm ischemic death rats.Then we use ischemic postcondi-tioning and adenosine postconditioning methods in the transplantation. 24 hours after transplantation we detect the change of the graft.Based on the data we evaluate the effects of these two methods and try to find the involving mechanisms.
Methods:The experiment includes three parts.
Part one:To set up a model of cervical heterotopic heart transplanta-tion in rats.
Part two:Study on the cardioprotection of ischemic postconditioning in cadaver donor rats with warm ischemia.Rats were randomly divided into seven groups.C group—control group.I_5、I_(15)、I_(30)group—simple warm ischemia group,CNBH received from the cadaver rats which were die from acute hemorrhagic shock and the warm ischemic durations are 5 min、15min and 30min separately.Then the CNBH were used to heart transplantation.P_5、P_(15)、P_(30)group—ischemic postconditioning group, after the heart transplanted as the simple warm ischemia group,the donor hearts were treated with ischemic postconditioning.24 hours after transplantation we detect the change of the grafts including pathologic damages,ATP、SOD、MDA、NF-κB mRNA、TNF-αIL-6、apoptosis level、Bcl-2 and Bax proteins.
Part three:Study on the cardioprotection of adenosine postconditioning in cadaver donor rats with warm ischemia.Rats were randomly divided into seven groups.C group—control group.I_5、I_(15)、I_(30) group—simple warm ischemia group,CNBH received from the cadaver rats which were die from acute hemorrhagic shock and the warm ischemic durations are 5 min、15min and 30min separately.Then the CNBH were used to heart transplantation.A_5、A_(15)、A_(30)group—adenosine postconditioning group,the CNBH were received as mentioned and treated with adenosine postconditioning before heart transplantation.24 hours after transplantation we detect the change of the grafts including pathologic damages、ATP、SOD、MDA、NF-κB mRNA、 TNF-αIL-6、apoptosis level、Bcl-2 and Bax proteins.
Result:1、The CNBH within 30min warm ischemia and 1h cold ischemia can be transplanted successfully.
2、With the prolonged warm ischemia duration,the ischemia/reper-fusion injury became more severe and the pathologic damage became worse.But at the same time point,compared with the simple warm ischemia group,the myocardial injury of the ischemic postconditioning group and the adenosine postconditioning group were attenuated. 3、At the same time point,compared with the simple warm ischemia group,the ischemic postconditioning group and the adenosine post-conditioning group can increase ATP and SOD in myocardial tissue, decrease MDA,NF-κB mRNA,TNF-α,IL-6.In addition,the decrease of apoptosis level,up-regulation of Bcl-2 protein and down-regulation of Bax protein can be detected in these two groups.
Conclusion:1、The CNBH within 30min warm ischemia and 1h cold ischemia can be transplanted successfully.
2、Ischemic postconditioning and adenosine postconditioning can protect the graft from ischemia-reperfusion injury in cadaver donor rats with warm ischemia.
3、The involving mechanisms may include that ischemic postcondi-tioning and adenosine postconditioning can improve myocardial energy metabolism,attenuate lipid peroxidation injury,suppress the expression of NF-κB mRNA,decrease the inflammatory damage of TNF-αand IL-6, up-regulation of Bcl-2 protein and down-regulation of Bax protein which lead to the shortage of myocardial cell apoptosis.
New ideas:
1、The study innovatively introduced the conception of postcondi-tioning into the area of heart transplantation.
2、We study on the cardioprotection of ischemic postconditioning in cadaver donor rats with warm ischemia for the first time.The similar researches were not reported.
3、We study on the cardioprotection of adenosine postconditioning in cadaver donor rats with warm ischemia for the first time.The similar researches were not reported.
Limitation:For the restriction of funds and equipments,we cannot evaluate the cardiac function of the graft,the detected data were limited and the observing duration was not long.
目的:本研究在首先建立大鼠颈部异位心脏移植模型的基础上,尝试对热缺血死亡后大鼠不同时段的供心,进行缺血后处理以及腺苷后处理,检测受体术后24小时移植心脏的相关指标,来评价其心脏保护作用并探讨可能机制。
方法:实验分为三大部分:
第一部分为大鼠颈部异位心脏移植模型的建立。
第二部分为缺血后处理对热缺血死亡大鼠供体心脏保护的研究。大鼠被随机分为7组:C组—对照组;I_5组、I_(15)组、I_(30)组—单纯热缺血组,供体大鼠失血性休克死亡后单纯热缺血5min、15min、30min取心移植组;P_5组、P_(15)组、P_(30)组—缺血后处理组,供体大鼠失血性休克死亡后热缺血5min、15min、30min取心移植并进行缺血后处理组。移植术后24小时取移植心脏标本,观察其病理改变,检测心甲橹疉TP、SOD、MDA、NF-κB mRNA、TNF-α、IL-6的含量,以及心肌细胞凋亡和Bcl-2、Bax蛋白的表达情况。
第三部分为腺苷后处理对热缺血死亡大鼠供体心脏保护的研究。大鼠被随机分为7组:C组—对照组;I_5组、I_(15)组、I_(30)组—单纯热缺血组,供体大鼠失血性休克死亡后单纯热缺血5min、15min、30min取心移植组;A_5组、A_(15)组、A_(30)组—腺苷后处理组,供体大鼠失血性休克死亡后热缺血5min、15min、30min取心移植并进行腺苷后处理组。移植术后24小时取移植心脏标本,观察其病理改变,检测心肌组织ATP、SOD、MDA、NF-κB mRNA、TNF-α、IL-6的含量,以及心肌细胞凋亡和Bcl-2、Bax蛋白的表达情况。
结果:
1、热缺血死亡30分钟以内,冷缺血1小时左右的大鼠CNBH可以被成功移植。
2、随着热缺血时间的延长,移植心脏的缺血/再灌注损伤越重,病理损害也越重;而在同一时间点与单纯热缺血组相比,缺血后处理组和腺苷后处理组心肌细胞损害被减轻。
3、在同一时间点,缺血后处理以及腺苷后处理与单纯热缺血组相比,可以增加心肌组织的ATP、SOD含量,减少其MDA含量;减少心肌组织的NF-κB mRNA的表达及TNF-α、IL-6的含量;减轻心肌细胞的凋亡水平、上调Bcl-2蛋白表达而下调Bax蛋白表达。
结论:
1、热缺血死亡30分钟以内,冷缺血1小时左右的大鼠CNBH可以被成功应用于心脏移植;
2、缺血后处理以及腺苷后处理对热缺血死亡大鼠心脏移植的供心缺血/再灌注损伤具有保护作用;
3、缺血后处理以及腺苷后处理的心脏保护作用可能与其改善供心的能量代谢、减轻脂质过氧化损伤、抑制NF-κB表达所致炎性损伤以及减少心肌细胞的凋亡有关。
创新点:
1、本实验创新性的将后处理的概念引入心脏移植领域;
2、本实验首次研究缺血后处理对热缺血死亡大鼠供体心脏保护的作用,国内外未见相关报道;
3、本实验首次研究腺苷后处理对热缺血死亡大鼠供体心脏保护的作用,国内外未见相关报道。
不足之处:由于经费、设备等多种限制,无法对移植后的供心进行功能上的检测、相关的检测指标尚不够全面、移植后的观察时间较短。
Background:With the development of transplantation,researchers must face a global problem—the shortage of donors.In order to enlarge the donor pool,some of them turn to non-heart-beating donors(NHBD) and attempt to use cadaver non-beating heart(CNBH)in the heart trans-plantation. Now they think the CNBH received from those who die from acute hemorrhagic shock may be useful.Because none preconditioning methods can be used before the heart stop beating.So we have to try some postconditioning methods to attenuate the warm ischemia and ischemia-reperfusion injury,and to improve the cardiac function after heart transplantation.
Objective:Firstly we try to set up a cervical heterotopic heart trans-plantation in warm ischemic death rats.Then we use ischemic postcondi-tioning and adenosine postconditioning methods in the transplantation. 24 hours after transplantation we detect the change of the graft.Based on the data we evaluate the effects of these two methods and try to find the involving mechanisms.
Methods:The experiment includes three parts.
Part one:To set up a model of cervical heterotopic heart transplanta-tion in rats.
Part two:Study on the cardioprotection of ischemic postconditioning in cadaver donor rats with warm ischemia.Rats were randomly divided into seven groups.C group—control group.I_5、I_(15)、I_(30)group—simple warm ischemia group,CNBH received from the cadaver rats which were die from acute hemorrhagic shock and the warm ischemic durations are 5 min、15min and 30min separately.Then the CNBH were used to heart transplantation.P_5、P_(15)、P_(30)group—ischemic postconditioning group, after the heart transplanted as the simple warm ischemia group,the donor hearts were treated with ischemic postconditioning.24 hours after transplantation we detect the change of the grafts including pathologic damages,ATP、SOD、MDA、NF-κB mRNA、TNF-αIL-6、apoptosis level、Bcl-2 and Bax proteins.
Part three:Study on the cardioprotection of adenosine postconditioning in cadaver donor rats with warm ischemia.Rats were randomly divided into seven groups.C group—control group.I_5、I_(15)、I_(30) group—simple warm ischemia group,CNBH received from the cadaver rats which were die from acute hemorrhagic shock and the warm ischemic durations are 5 min、15min and 30min separately.Then the CNBH were used to heart transplantation.A_5、A_(15)、A_(30)group—adenosine postconditioning group,the CNBH were received as mentioned and treated with adenosine postconditioning before heart transplantation.24 hours after transplantation we detect the change of the grafts including pathologic damages、ATP、SOD、MDA、NF-κB mRNA、 TNF-αIL-6、apoptosis level、Bcl-2 and Bax proteins.
Result:1、The CNBH within 30min warm ischemia and 1h cold ischemia can be transplanted successfully.
2、With the prolonged warm ischemia duration,the ischemia/reper-fusion injury became more severe and the pathologic damage became worse.But at the same time point,compared with the simple warm ischemia group,the myocardial injury of the ischemic postconditioning group and the adenosine postconditioning group were attenuated. 3、At the same time point,compared with the simple warm ischemia group,the ischemic postconditioning group and the adenosine post-conditioning group can increase ATP and SOD in myocardial tissue, decrease MDA,NF-κB mRNA,TNF-α,IL-6.In addition,the decrease of apoptosis level,up-regulation of Bcl-2 protein and down-regulation of Bax protein can be detected in these two groups.
Conclusion:1、The CNBH within 30min warm ischemia and 1h cold ischemia can be transplanted successfully.
2、Ischemic postconditioning and adenosine postconditioning can protect the graft from ischemia-reperfusion injury in cadaver donor rats with warm ischemia.
3、The involving mechanisms may include that ischemic postcondi-tioning and adenosine postconditioning can improve myocardial energy metabolism,attenuate lipid peroxidation injury,suppress the expression of NF-κB mRNA,decrease the inflammatory damage of TNF-αand IL-6, up-regulation of Bcl-2 protein and down-regulation of Bax protein which lead to the shortage of myocardial cell apoptosis.
New ideas:
1、The study innovatively introduced the conception of postcondi-tioning into the area of heart transplantation.
2、We study on the cardioprotection of ischemic postconditioning in cadaver donor rats with warm ischemia for the first time.The similar researches were not reported.
3、We study on the cardioprotection of adenosine postconditioning in cadaver donor rats with warm ischemia for the first time.The similar researches were not reported.
Limitation:For the restriction of funds and equipments,we cannot evaluate the cardiac function of the graft,the detected data were limited and the observing duration was not long.
引文
[1] Garrity ER, Moore J, Mulligan MS, et al. Heart and lung transplantation in the United States, 1996-2005. Am J Transplant 2007;7:1390-403
[2] Taylor DO, Edwards LB, Boucek MM, et al. Registry of the International Society for Heart and Lung Transplantation: twenty-fourth official adult heart transplant report 2007. J Heart Lung Transplant 2007;26:769-81
[3] Evers KA, Lewis DD. Estimating the non-heart-beating donor potential at a trauma center. J Transpl Coord 1999;9:186
[4] del Rio Gallegos F, Nunez Pena JR, Soria Garcia A, et al. Non heart beating donors. Successfully expanding the donor's pool. Ann Transplant 2004;9:19
[5] Sanchez-Fructuoso Al, Prats D, Torrente J, et al. Renal transplantation from non-heart-beating donors: a promising alternative to enlarge the donor pool. J Am SocNephrol 2000;11:350
[6] Ad Hoc Committee of the Harvard Medical School to Examine the Definition of Brain Death: A definition of irreversible coma. Report of the Ad Hoc Committee of the Harvard Medical School to Examine the Definition of Brain Death. JAMA 1968;205:337
[7] Belzer FO, Salvatierra 0 Jr. The organization of an effective cadaver renal transplantation program. Transplant Proc 1974;6:93
[8] Calne RY, Loughridge L, MacGillivray JB, et al. Further observations on renal transplants in man from cadaveric donors. Brit Med J 1966;2:1345
[9] Mowbray JF, Cohen SL, Doak PB, et al. Human cadaveric renal transplantation:Report of twenty cases. Br Med J 1965;2:1387
[10] Pletka P, Cohen SL, Hulme B, et al. Cadaveric renal transplantation: An analysis of 165 cases. Lancet 1969;1:1
[11] Hall CL, SansomJR, Obeid M, et al. Agonal phase, ischemic times, and renal vascular abnormalities and outcome of cadaver kidney transplants. Br Med J1975;3:667
[12]Marks WH,Wagner D,Pearson TC,et al.Organ donation and utilization,1995-2004:Entering the collaborative era.Am J Transplantation 2006;6:1101
[13]Hattori R,Ono Y,Yoshimura N,et al.Long term outcome of kidney transplant using non-heart-beating donor:Multicenter analysis of factors affecting graft survival.Clinical Transplantation 2003;17:6 518-521
[14]Dubbeld J,Porte R,Hoek v B,et al.non-heart-beating donor liver transplantation:Experience in the netherlands after introdution of restrictive national protocol.Liver Transplantation 2007;13:6 S195
[15]Dark JH.Lung transplantation from the non-heart-beating donor.Transplantation 2008;86(2)200-201
[16]Kootstra G,Daemen JHC,Oomen APA.Categories of non-heart-beating donors.Transplant Proc 1995;27:2893-4
[17]H.Myron Kauffmana,John D Rosendalea,Sarah E Taranto,et al.Non-heart-beating donors(then)and donation after cardiac death(now).Transplant Rev 2007;21:237-248
[18]Begona JA,Gundry SR,Razzouk,et al.Transplantation of hearts after arrest and resuscitation,early and long term results.J Thorac Cardiovasc Surg 1993;106:1196-201
[19]Michael J.Collins,Sina L Moainie,Bartley P Griffith,et al.Preserving and evaluating hearts with ex vivo machine perfusion:an avenue to improve early graft performance and expand the donor pool.Euro J Cardio-thoracic Surg 2008;34:318-325
[20]龚斌,朱家麟,张宝仁,等.窒息死亡尸体心脏移植复苏的实验研究.第二军医大学学报 1999;20(12):1043-1045
[21]Abbott CP,Lindsey ES,Creech O J r,et al.A technique for heart transplantation in the rat.Arch Surg 1964;89:645-652
[22]Ono K,Lindsey ES.Improved technique of heart transplantation in rats.J Thorac Cardiovasc Surg 1969;57(2):225-229
[23]Heron I.A technique for accessory cervical heart transplantation in rabbits and rats.Acta Pathol Microbiol Scand A Pathol 1971;79:366
[24]李志勇,孙建宁,张硕峰.水合氯醛和戊巴比妥钠对SD大鼠麻醉效果的比较.四川动物 2008;2:299-302
[25]程晓峰,景华,胡小南,等.建立大鼠心脏移位移植模型的麻醉选择.医学研究生学报 2005;18(10):958-959
[26]顾晓,赵鸿,古涛.两种大鼠异位心脏移植模型的制备.复旦大学学报:医学版 2007;34(3):572-575
[27]叶文学,沈振亚,张胜超.高复跳率小鼠颈部异位心脏移植模型的建立.实验动物与比较医学 2008,28(3):148-150
[28]尤颢,廖崇先,赵霞,等.大鼠异位心脏移植模型手术的改良.兰州大学学报:医学版 2008,34(3):9-11
[29]Xiu DR,Uchida H,To H,et al.Simplified method of heterotopic rat heart trans-plantation using the cuff technique:Application to sub lethal dose protocol of methotrexate on allograft survival.Microsurgery 2001;21(1):16-21
[30]苏刚,孙宗全,董念国,等.袖套法小鼠颈部异位心脏移植模型的建立.新乡医学院学报 2006;23(5):534-734
[31]Zhao ZQ,Corvera JS,Halkos ME,et al.Inhibition of myocardial injury by ischemic postconditioning during reperfusion:comparison with ischemic preconditioning.Am J Heart Circ Physiol 2003;285:H579-H588
[32]Kin H,Zhao ZQ,Sun HY,et al.Postconditioning attenuates myocardial ischemia reperfusion injury by inhibiting events in the early minutes of reperfusion.Cardiovasc Res 2004;62:74-85
[33]Yang XM,Proctor JB,Cui L,et al.Multiple,brief coronary occlusions during early reperfusion protect rabbit hearts by targeting cell signaling pathways.J Am Coll Cardiol 2004;44(5):1103-1110
[34]Iliodromitis EK,Georgiadis M,Cohen MV,et al.Protection from postconditioning depends on the number of short ischemic insults in anesthetized pigs.Basic Res Cardiol 2006;101:502-507
[35]Bopassa JC,Ferrera R,Gateau Roesch O,et al.PI-3 kinase regulates the mitochondrial transition pore in controlled reperfusion and postconditioning.Cardiovasc Res 2006;69:178-185
[36]Staat P,Rioufol G,Piot C,et al.Postconditioning the human heart.Circulation 2005;112:2143-8
[37]Laskey WK.Brief repetitive balloon occlusions enhance reperfusion during percutaneous coronary intervention for acute myocardial infarction:a pilot study.Catheter Cardiovas Interv 2005;65:361-7
[38]Luo W,Li B,Chen R,et al.Effect of ischemic postonditioning in adult valve replacement.Eur J Cardiothorac Surg 2008 Feb;33(2):203-8
[39]Glanemann M,Langrehr JM,Stange B J,et al.Clinical implications of hepatic preservation injury after adult liver transplantation.Am J Transplant 2003;3:1003-9
[40]Mueller AR,Platz KP,Haak M,et al.The release of cytokines,adhesion molecules,and extracellular matrix parameters during and after reperfusion in human liver transplantation.Transplantation 1996;62:1118-26
[41]Murry CE,Jenningsx CE,Reimer KA.Preconditioning with ischemia:a delay of lethal cell injury in ischemic myocardium.Circulation 1986;74:1124-36
[42]Landymore RW,Bayes A J,Murphy JT,et al.Preconditioning prevents myocardial stunning after cardiac transplantation.Ann Thorac Surg 1998;66:1953-7
[43]Jassem W,Fuggle SV,Cerundolo L,et al.Ischemic preconditioning of cadaver donor livers protects allografts following transplantation.Transplantation 2006;81:169-74
[44]牛英,叶启发.缺血后处理及其在器官移植术中的应用.中南大学学报(医学版)2008;33(6):548-552
[45]马兰,李力兵,高长青,等.离体供心保存技术的研究现状.中国体外循环杂志 2008;6(4)255-256
[46]Ambrosio G,Zweier JL,Flaherty JT.The relationship between oxygen radical generation and impairment of myocardial energy metabolism following postischemic reperfusion.J Mol Cell Cardiol 1991;23:1359-1374
[47]Kevin LG,Camara AKS,Riess ML,et al.Ischemic preconditioning alters realtime measure of O_2 radicals in intact hearts with ischemia and reperfusion.Am J Physiol(Heart Circ Physiol)2003;284:H566-H574
[48]Scholz W,Albus U,Linz W,et al.Effect of Na~+/H~+exchange inhibitors in cardiac ischemia.J Mol Cell Cardiol 1992;24:731-740
[49]Jordan JE,Zhao ZQ,Vinten-Johansen J.The role of neutrophils in myocardial ischemia-reperfusion injury.Cardiovasc Res 1999;43:860-878
[50]Lefer AM,Tsao PS,Lefer DJ,et al.Role of endothelial dysfunction in the pathogenesis of reperfusion injury after myocardial ischemia.FASEB J 1991;5:2029-2034
[51]Sun HY,Wang NP,Kerendi F,et al.Hypoxic postconditioning reduces cardiomyocyte loss by inhibiting ROS generation and intracellular Ca~(2+)overload.Am J Physiol 2005;288:H1900-H1908
[52]Fujita M,Asanuma H,Hirata A,et al.Prolonged transient acidosis during early reperfusion contributes to the cardioprotective effects of postconditioning.Am J Physiol Heart Circ Physiol 2007;292(4):2004-2008
[53]姚树桐,李玉珍,刘秀华,等.缺血后处理对小肠缺血再灌注损伤大鼠肠系膜微循环的影响.微循环学杂志 2007;17(2):1-4
[54]郭晓笋,刘秀华,张振英,等.缺血后处理通过改善微循环减轻大鼠骨骼肌缺血再灌注损伤.微循环学杂志 2007;17(4):8-11
[55]Zhao ZQ,Sun HY,Wang NP,et al.Hypoxic postconditioning attenuates cardiomyocyte apoptosis via inhibition ofjnk and p38 kinases pathway.J Mol Cell Cardiol 2005;38:870
[56]Andrew P Halestrap,Philippe Pasdois.The role of the mitochondrial permeability transition pore in heart disease.Biochim Biophys Acta 2009;(In Press)
[57]Hall G,Hasday JD,Rogers TB.Regulating the regulator:NF-kappa B signaling in the heart.J Mol Cell Cardiol 2006;41:580-91
[58]Jones WK,Brown M,Wilhide M,et al.NF-kappa B in cardiovascular disease:diverse and specific effects of a“general”transcription factor? Cardio vasc Toxicol 2005;5:183-202
[59]Valen G,Yan ZQ,Hansson GK.Nuclear factor kappa-B and the heart.J Am Coll Cardiol 2001;38:307-14
[60]Chandrasekar B,Freeman GL.Induction of nuclear factor kappa B and active- tion protein 1 in postischemic myocardium. FEBS Lett 1997;401:30-4
[61] Li C, Browder W, Kao RL. Early activation of transcription factor NF kappa B during ischemia in perfused rat heart. Am J Physiol 1999;276:H543-52
[62] Li C, Kao RL, Ha T, et al. Early activation of IKKbeta during in vivo myocardial ischemia. Am J Physiol 2001;280:H1264-71
[63] Zhang C. The role of inflammatory cytokines in endothelial dysfunction. Basic Res Cardiol 2008;103(5):398-406
[64] Dorge H, Schulz R, Belosjorow S, et al. Coronary microembolization: the role of TNF-alpha in contractile dysfunction. J Mol Cell Cardiol 2002;34(l):51-62
[65] Schulz R, Aker S, Belosjorow S, et al. TNF alpha in ischemia/reperfusion injury and heart failure. Basic Res Cardiol 2004;99(1):8-11
[66] Chandra J, Samali A, Orrenius S. Triggering and modulation of apoptosis by oxidative stress. Free Radic Biol Med 2000;29:323
[67] Yang S, Zheng R, Hu S, et al. Mechanism of cardiac depression after trauma-hemorrhage: increased cardiomyocyte IL-6 and effect of sex steroids on IL-6 regulation and cardiac function. Am J Physiol: Heart Circ Physiol 2004; 287:H2183-91
[68] Ikeda U, Ohkawa F, Seino Y, et al. Serum interleukin 6 levels become elevated in acute myocardial infarction. J Mol Cell Cardiol 1992;24:579-84
[69] Kin H, Wang NP, Mykytenko J, et al. Inhibition of myocardial apoptosis by postconditioning is associated with attenuation of oxidative stress-mediated nuclear factor-kappa B translocation and TNF alpha release. Shock 2008 Jun;29(6):761 -8
[70] Fliss H, Gattinger D. Apoptosis in ischemic and reperfused rat myocardium.Circ Res 1996;79(5):949
[71] Inserte J, Tairmor G, Hof staetter B, et al. Influence of simulated ischemia on apoptosis induction by oxidative stress in adult cardiomyocytes of rats. Am J Physiol Heart Circ Physiol 2000;278(1):94-99
[72] JS Kim, Y Jin, JJ Lemasters. Reactive oxygen species, but not Ca~(2+) over loading, trigger pH and mitochondrial permeability transition-dependent death of adult rat myocytes after ischemia-reperfusion.Am J Physiol 2006;290:H2024-H2034
[73]Kim JS,He L,Lemasters JJ.Mitochondrial permeability transition:a common pathway to necrosis and apoptosis.Biochem Biophys Res Commun 2003;304:463-470
[74]姚树桐,刘秀华,王家富.缺血后处理的心肌保护机制研究进展.微循环学杂志 2008;18(1):49-52
[75]Knudson CM,Korsmeyer SJ.Bcl-2 and bax function independently to regulate cell death.Nat Genet 1997;16(4):358
[76]Antonsson B,Conti F,Ciavat ta A,et al.Inhibition of bax channel forming activity by bcl-2.Science 1997;277(5324):370
[77]Naumovski L,Cleary ML.The p53-binding 53 BP2 also interacts with bcl-2and impedes cell cycle progression at G2/M.Mol Cell Biol 1996;16:3884
[78]Adams JM,Cory S.Life-or-death decisions by the Bcl-2 protein family.Trends Biochem Sci 2001;26:61-66
[79]吴青,陶宏凯,陶大昌,等.灌注诱导心肌细胞凋亡及凋亡相关基因表达的研究.中国心血管病研究杂志 2004;2(11):905
[80]Borutaite V,Brown GC.Mitochondria in apoptosis of ischemic heart.FEBS Lett 2003;541(123):1
[81]Dwaine S Burley,Gary F Baxter.Pharmacological targets revealed by myocardial postconditioning.Curr Opin Pharmacol 2008;Dec:(In Press)
[82]Pitarys C J,Virmani R,Vildibill HD Jr,et al.Reduction of myocardial reperfusion injury by intravenous adenosine administered during the early reperfusion period.Circulation 1991;83:237-247
[83]Kin H,Lofye MT,Amerson BS,et al.Cardioprotection by“postconditioning” is mediated by increased retention of endogenous intravascular adenosine and activationof A_(2a)receptors during reperfusion.Circulation 2004;110:Ⅲ-168
[84]Fryer RM,Auchampach JA,Gross GJ.Therapeutic receptor targets of ischemic preconditioning.Cardiovasc Res 2002;55:520-5
[85]Michael V Cohen,James M Downey.Adenosine at reperfusion:A conundrum ready to be resolved. J Am Coll Cardiol 2009 Feb 24;53(8):718-9
[86] Schulte G, Fredholm BB. Signalling from adenosine receptors to mitogen-activateed protein kinases. Cell Signal 2003; 15:813-827
[87] Mubagwa K, Flameng W. Adenosine, adenosine receptors and myocardial protection: an updated overview. Cardiovasc Res 2001 ;52:25-39
[88] Jason N Peart, John P Headrick. Adenosinergic cardioprotection: Multiple receptors, multiple pathways. Pharmaco Ther 2007; 114:208-221
[89] Kilpatrick EL, Narayan P, Mentzer RM Jr, et al. Cardiacmyocyte adenosine A2a receptor activation fails to alter cAMP or contractility: role of receptor localization. Am J Physiol 2002;282:H1035-H1040
[90] David Ribe, David Sawbridge, Sapna Thakur, et al. Adenosine A_(2A) receptor signaling regulation of cardiac NADPH oxidase activity. Free Radic Biol Med 2008;44:1433-1442
[91] Nolte D, Lorenzen A, Lehr HA, et al. Reduction of postischemic leukocyte endothelium interaction by adenosine via A2 receptor. Naunyn Schmiedebergs Arch Pharmacol 1992;346:234-7
[92] Zhao ZQ, Sato H, Williams MW, et al. Adenosine A2-receptor activation inhibits neutrophil-mediated injury to coronary endothelium. Am J Physiol 1996;271:H1456-64
[93] Aleksander Jovanovic', Alexey E Alekseev, Jo'se R Lo' pez, et al. Adenosine prevents hyperkalemia-induced calcium loading in cardiac cells: Relevance for cardioplegia. Ann Thorac Surg 1997;63:153-61
[94] Zhao ZQ, Budde J M., Morris C D, et al. Adenosine attenuates reperfusion-induced apoptotic cell death by modulating expression of Bcl-2 and Bax proteins. J Mol Cell Cardiol 2001;33:57-68
[95] Yang XM, Philipp S, Downey JM, et al. Postconditioning's protection is not dependent on circulating blood factors or cells but involves adenosine receptors and requires PI3-kinase and guanylyl cyclase activation. Basic Res Cardiol 2005;100:57-63
[96] Kin H, Zatta AJ, Lofye MT, et al. Postconditioning reduces infarct size via adenosine receptor activation by endogenous adenosine.Cardiovasc Res 2005;67:124-133
[97]Philipp S,Yang XM,Cui L,et al.Postconditioning protects rabbit hearts through a protein kinase C-adenosine A2b receptor cascade.Cardiovasc Res 2006;70:308-314
[98]Takahama H,Minamino T,Asanuma H,et al.Prolonged targeting of ischemic/reperfused myocardium by liposomal adenosine augments cardioprotection in rats.J Am Coll Cardiol 2009;53:709-17
[99]Pitarys CJ Ⅱ,Virmani R,Vildibill HD Jr,et al.Reduction of myocardial reperfusion injury by intravenous adenosine administered during the early reperfusion period.Circulation 1991;83:237-47
[100]Jason M Budde,Cullen D Morris,Daniel A Velez,et al.Reduction of infarct size and preservation of endothelial function by multidose intravenous adenosine during extended reperfusion.J Surg Res 2004;116,104-115
[101]Goto M,Miura T,Iliodoromitis EK,et al.Adenosine infusion during early reperfusion failed to limit myocardial infarct size in a collateral deficient species.Cardiovasc Res 1991;25:943-9
[102]Claudia Penna,Daniele Mancardi,Francesca Tullio,et al.Intermittent adenosine at the beginning of reperfusion does not trigger cardioprotection.J Surg Res 2008;(In Press)
[103]Thourani VH,Ronson RS,Van Wylen DG,et al.Adenosine-supplemented blood cardioplegia attenuates postischemic dysfunction after severe regional ischemia.Circulation 1999;100:Ⅱ376-83
[104]李芝,邵永丰,梁永,等.腺苷在心脏直视术中心肌保护作用的研究.中国体外循环杂志 2008;6(3):149-151
[105](?)yvind Jakobsen,Stig Muller,Erling Aarsaether,et al.Adenosine instead of supranormal potassium in cardioplegic solution improves cardioprotection.Eur J Cardiothorac Surg 2007;32:493-500
[1] Jennings RB, Sommer HM, Smyth GA, et al. Myocardial necrosis induced by temporary occlusion of a coronary artery in the dog. Arch Pathol 1960;70:68-78
[2] Goldhaber JI, Weiss JN. Oxygen free radicals and cardiac reperfusion abnormalities. Hypertension 1992;20:l 18-127
[3] Jacob Vinten-Johansen. Postconditioning: a mechanical maneuver that triggers biological and molecular cardioprotective responses to reperfusion. Heart Fail Rev 2007; 12:235-244
[4] Becker LC, Ambrosio G. Myocardial consequences of reperfusion. Prog Cardio vasc Dis 1987;30:23-44
[5] Forman MB, Virmani R, Puett DW. Mechanisms and therapy of myocardial reperfusion injury. Circulation 1990;81(suppl Ⅳ):Ⅳ-69-78
[6] Hearse DJ, Bolli R. Reperfusion induced injury: manifestations, mechanisms,and clinical relevance. [Review]. Cardiovasc Res 1992;26:101-8
[7] Jeroudi MO, Hartley CJ, Bolli R. Myocardial reperfusion injury: role of oxygen radicals and potential therapy with antioxidants. [Review]. Am J Cardiol 1994;73:2B-7B
[8] Jordan JE, Zhao ZQ, Vinten-Johansen J. The role of neutrophils in myocardial ischemia-reperfusion injury. Cardiovasc Res 1999;43: 860-78
[9] Lucchesi BR. Complement, neutrophils and free radicals: mediators of reperfusion injury. [Review]. Arzneim-Forsch/Drug Res 1994;44:420-32
[10] Opie LH. Role of calcium and other ions in reperfusion injury. Cardiovasc Drugs Ther 1991;5:237-47
[11] Piper HM, Meuter K, Schafer C. Cellular mechanisms of ischemia-reperfusion injury. Ann Thorac Surg 2003;75:S644-8
[12] Jean Pierre Monassier. Reperfusion jnjury in acute myocardial infarction: From bench to Cath lab. Part I : Basic considerations. Arch Cardiovas Dis 2008;101(7-8):491-500
[13] Murry CE, Jennings RB, Reimer KA. Preconditioning with ischemia: A delay of lethal cell injury in ischemic myocardium. Circulation 1986;74:1124-1136
[14] Zhao ZQ, Corvera JS, Halkos ME, et al. Inhibition of myocardical injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. Am J Heart Circ Physiol 2003;285:H579-H588
[15] Kin H, Zhao ZQ, Sun HY, et al. Postconditioning attenuates myocardial ischemia-reperfusion injury by inhibiting events in the early minutes of reperfusion. Cardiovasc Res 2004;62:74-85
[16] Yang XM, Proctor JB, Cui L, et al. Multiple, brief coronary occlusions during early reperfusion protect rabbit hearts by targeting cell signaling pathways. J Am Coll Cardiol 2004;44(5):1103-1110
[17] Iliodromitis EK, Georgiadis M, Cohen MV, et al. Protection from postconditioning depends on the number of short ischemic insults in anesthetized pigs.Basic Res Cardiol 2006; 101:502-507
[18] Bopassa JC, Ferrera R, Gateau Roesch O, et al. PI-3 kinase regulates the mitochondrial transition pore in controlled reperfusion and postconditioning. Cardiovasc Res 2006;69:178-185
[19] Sun HY, Wang NP, Kerendi F, et al. Hypoxic postconditioning reduces cardio-myocyte loss by inhibiting ROS generation and intracellular Ca~(2+) overload. Am J Physiol 2005;288:H1900-8
[20] K Sun, ZS Liu, Q Sun. Role of mitochondria in cell apoptosis during hepatic ischemia-reperfusion injury and protective effect of ischemic postconditioning. World J Gastroenterol 2004; 10:1934-1938
[21] Eldaif SM, Geneve J, Wang NP, et al. Postconditioning beyond the heart: Post conditioning the ischemic kidney attentutes renal reperfusion injury. Circulation 2007; 116(16) :61-62
[22] H Zhao, RM Sapolsky, GK Steinberg. Interrupting reperfusion as a stroke therapy: ischemic postconditioning reduces infarct size after focal ischemia in rats. J Cereb Blood Flow Metab 2006;26:1114-1121
[23] dos Santos CHM, Gomes OM, Pontes JCDV, et al. The ischemic preconditioning and postconditioning effect on the intestinal mucosa of rats undergoing the ot mesenteric ischemia/reperfusion procedure.Acta Cirugica Brasileira 2008;23:22-28
[24]Wu XD,Zhang ZY,Liu XH,et al.Ischemic postconditioning protects skeletal muscle from reperfusion injury through calreticulin regulated.J of Amer Colle of Cadio 2008;51-10:B75
[25]Kerendi F,Kin H,Halkos ME,et al.Remote postconditioning.Brief renal ischemia and reperfusion applied before coronary artery reperfusion reduces myocard ial infarct size via endogenous activation of adenosine receptors.Basic Res Cardiol 2005;100:404-12
[26]袁志柳,刘兴德,陈保林等.缺血后处理对缺血再灌注大鼠心肌梗死面积、CK、MDA及SOD的影响.微循环学杂志 2006;16:27-28,31
[27]杨国杰,李运伟,曾秋棠等.缺血后处理对兔缺血再灌注心肌细胞凋亡及Bcl -2和Bax蛋白表达的影响.郑州大学学报(医学版)2008;43:57-59
[28]郭晓笋,刘秀华,张振英等.缺血后处理通过改善微循环减轻大鼠骨骼肌缺血再灌注损伤.微循环学杂志 2007;17(4):8-11.
[29]郑鸣之,蒋建平,陈莹莹等.缺血后处理对不同时程冷保存大鼠心脏的作用研究.浙江大学学报(医学版)2007;36(6):567-574
[30]Galagudza M,Kurapeev D,Minasian S,et al.Ischemic postconditioning:brief ischemia during reperfusion converts persistent ventricular fibrillation into regular rhythm.Eur J Cardio-Thorac Surg 2004;25:1006-10
[31]Desagher S,Martinou JC.Mitochondria as the central contral point of apoptosis.Trends Cell Biol 2000;10(9):369-377
[32]Zhao ZQ,Sun HY,Wang NP,et al.Hypoxic postconditioning attenuates cardio myocyte apoptosis via inhibition ofjnk and p38 kinases pathway.J Mol Cell Cardiol 2005;38:870
[33]Philipp SD,Downey JM,Cohen MV.Postconditioning must be initiated in less than l minute following reperfusion and is dependent on adenosine receptors and P13-kinase.Circulation 2004;110:Ⅲ-168
[34]Burda J,Danielisova V,Nemethova,M,et al.Delayed postconditionig initiates additive mechanism necessary for survival of selectively vulnerable neurons after transient ischemia in rat brain. Cell Mol Neurobiol 2006;26(7-8): 1141-1151
[35] Zhao ZQ, Jakob Vinten-Johansen. Postconditioning: Reduction of reperfusion induced injury. Cardiovasc Res 2006;70:200-211
[36] Mykytenko J, Kerendi F, Reeves JG, et al. Long-term inhibition of myocardial infarction by postconditioning during reperfusion. Basic Res Cardiol 2007; 102:90-100.
[37] Mykytenko J, Reeves JG, Kin H, et al. Postconditioning reduces infarct size via mitochondrial K_(Atp) channel activation during 24 hours of reperfusion. J Mol Cell Cardiol 2005;38:830
[38] Andreka G, Vertesaljai M, Szantho G, et al. Remote ischemic postconditioning protects the heart during acute myocardial infarction of pigs. Heart 2007; 93:749-752
[39] Argaud L, Gateau-Roesch O, Raisky O, et al. Post conditioning inhibits mitochondrial permeability transition. Circulation 2005; 111:194-197
[40] Vinten-Johansen Jakob, Kin Hajime, Sun He Ying, et al. Postconditioning reduces myocardial injury by inhibiting reactive oxygen species during reperfusion. Circulation 2003; 108(17): Ⅳ-219
[41] Engelman DT, Watanabe M, Engleman RM, et al. Constitutive nitric oxide release is impaired after ischemia and reperfusion. J Thorac Cardiovasc Surg1995;110:1047-53
[42] Ma X-L, Weyrich AS, Lefer DJ, et al. Diminished basal nitric oxide release after myocardial ischemia and reperfusion promotes neutrophil adherence to coronary endothelium. Circ Res 1993;72:403-12
[43] Palazzo AJ, Jones SP, Anderson DC, et al. Coronary endothelial P-selectin in pathogenesis of myocardial ischemia injury. Am J Physiol (Heart Circ Physiol) 1998;275:H1865-72
[44] Weyrich AS, Ma X-L, Lefer DJ, et al. In vivo neutralization of P-selectin protects feline heart and endothelium in myocardial ischemia and reperfusion injury.J Clin Invest 1993;91:2620-9
[45]Scholz W,Albus U,Linz W,et al.Effect of Na~+/H~+exchange inhibitors in cardiac ischemia.J Mol Cell Cardiol 1992;24:731-740
[46]姚树桐,李玉珍,刘秀华,等.缺血后处理对小肠缺血再灌注损伤大鼠肠系膜微循环的影响.微循环学杂志2007;17(2):1-4
[47]Keith A Webster.Programmed death as a therapeutic target to reduce myocardial infarction.Trends Pharmacol Sci 2007;28(9):492-499
[48]Yamaguchi H,Wang HG:The protein kinase PKB/Akt regulates cell survival and apoptosis by inhibiting Bax conformational change.Oncogene 2001,20:7779-7786
[49]Cronstein BN,Kramer SB,Weissmann G,et al.Adenosine:a physiological modulator of superoxide anion generation by human neutrophils.J Exp Med 1983;158:1160-77
[50]Kitakaze M,Hori M,Sato H,et al.Endogenous adenosine inhibits platelet aggregation during myocardial ischemia in dogs.Circ Res 1991;69:1402-8
[51]Colli S,Tremoli E.Multiple effects of dipyridamole on neutrophils and mononuclear leukocytes:adenosine dependent and adenosine-independent mechanisms.J Lab Clin Med 1991;118:136-45
[52]Williams MW,Jordan JE,Fernandez AZ,et al.Adenosine(ADO)inhibits unactivated neutrophil(PMN)adherence to thrombin stimulated coronary vascular endothelium(EC)by a p-selectin mechanism.FASEB J 1996;10:280
[53]Cronstein BN,Levin RI,Philips M,et al.Neutrophil adherence to endothelium is enhanced viaadenosine Al receptors and inhibited via adenosine A2receptors.J Immunol 1992;148:2201-6
[54]Nakamura M,Zhao Z-Q,Clark KL,et al.A novel adenosine analog,AMP579,inhibits neutrophil activation,adherence and neutrophil-mediated injury to coronary vascular endothelium.Eur J Pharm 2000;397:197-205
[55]Nolte D,Lehr HA,Messmer K.Adenosine inhibits postischemic leukocyte-endothelium interaction in postcapillary venules of the hamster.Am J Physiol 1991;261:H651-5
[56] Philipp S, Yang XM, Cui L, et al. Postconditioning protects rabbit hearts through a protein kinase C-adenosine A2b receptor cascade. Cardiovasc Res2006;70:308-314
[57] Lefer DJ, Nakanishi K, Vinten-Johansen J, et al. Cardiac venous endothelial dysfunction after myocardial ischemia and reperfusion in dogs. Am J Physiol 1992; 263:H850-6
[58] Tsao PS, Aoki N, Lefer DJ, et al. Time course of endothelial dysfunction and myocardial injury during myocardial ischemia and reperfusion in the cat. Circulation 1990;82:1402-12
[59] Johnson Ⅲ G, Tsao PS, Lefer AM. Cardioprotective effects of authentic nitric oxide in myocardial ischemia with reperfusion. Crit Care Med 1991; 19:244-52
[60] Pagliaro PR, Rastaldo R, Penna C, et al. Nitric oxide (NO)-cyclic guanosine monophosphate (cGMP) pathway is involved in ischemic postconditioning in the isolated rat heart. Circulation 2004; 110:111-136
[61] Ventura C, Bastagli L, Bernardi P, et al. Opioid receptors in rat cardiac sarcolemma: effect of phenylephrine and isoproterenol. Biochim Biophys Acta 1989;987: 69-74
[62] Wittert G, Hope P, Pyle D. Tissue distribution of opioid receptor gene expression in the rat. Biochem Biophys Res Commun 1996;218:877-81
[63] Kin H, Zatta AJ, Jiang R, et al. Activation of opioid receptors mediates the infarct size reduction by postconditioning. J Mol Cell Cardiol 2005;38:827
[64] Bolli R. Oxygen-derived free radicals and myocardial reperfusion injury: an overview. Cardiovasc Drugs Ther 1991;5(Suppl2):249-68
[65] Herkert O, Diebold I, Brandes RP, et al. NADPH oxidase mediates tissue factor-dependent surface procoagulant activity by thrombin in human vascular smooth muscle cells. Circulation 2002; 105:2030-6
[66] Penna C, Rastaldo R, Mancardi D, et al. Post-conditioning induced ardioprotec- tion requires signaling through a redox-sensitive mechanism, mitochondrial ATP sensitive K~+ channel and protein kinase C activation. Bas Res Cardiol 2006 Mar; 101(2): 180-9
[67] Marceau F, Hess JF, Bachvarov DR. The B1 receptors for kinins. Pharmacol Rev 1998;50:357-86
[68] Tschope C, Heringer Walther S, Koch M, et al. Myocardial bradykinin B2 receptor expression at different time points after induction of myocardial infarcttion. J Hyperten 2000; 18:223-8
[69] Bell RM, Yellon DM. Bradykinin limits infarction when administered as an adjunct to reperfusion in mouse heart: the role of PI3K. Akt and eNOS. J Mol CellCardiol2003;35:185-193
[70] Penna C, Mancardi D, Rastaldo R, et al. Intermittent activation of bradykinin B2 receptors and mitochondrial K_(Atp) channels trigger cardiac postcondition- ing through redox signaling. Cardiovasc Res 2007;75:168-177
[71] Penna C, Mancardi D, Tullio F, et al. Postconditioning and intermittent bradykinin induced cardioprotection require cyclooxygenase activation and prostacyclin release during reperfusion. Basic Res Cardiol 2008, 103:368-377
[72] Kis A, Yellon DM, Baxter GF. Role of nuclear factor- _KB activation in acute ischemia-reperfusion injury in myocardium. Br J Pharmacol 2003; 138:894
[73] Cargnoni A, Ceconi C, Gaia G, et al. Cellular thiols redox status: A switch for NF-_kB activation during myocardial post-ischaemic reperfusion. J Mol Cell Cardiol 2002;34:997
[74] M Zhang, YJ Xua, Harjot K, Sainia, et al. TNF-a as a potential mediator of cardiac dysfunction due to intracellular Ca~(2+)-overload. Biochem Biophys Res Commun 2005;327:57-63
[75] Kin H, Wang NP, Mykytenko J, et al. Inhibition of myocardial apoptosis by postconditioning is associated with attenuation of oxidative stress-mediated nuclear factor-kappa B translocation and TNF alpha release. Shock 2008 Jun;29(6):761-8
[76] Jobe LJ, Jiang R, Wang N-P, et al. Tissue factor, factors Ⅶa and Xa expression and local generation of thrombin in at risk myocardium occurs specifically during reperfusion. Circulation 2004;l 10:111-297
[77] Mackman N. The role of the tissue factor-thrombin pathway in cardiac ischemia-reperfusion injury. Semin Vasc Med 2003 ;3:193-8
[78] Jiang R, Reeves JG, Mykytenko J, et al. Postconditioning reduces reperfusion injury by inhibiting the tissue factor-thrombin pathway in a closed-chest porcine modelof ischemia-reperfusion. Circulation 2005;112(Suppl Ⅱ):Ⅱ-309
[79] Cantley LC. The phosphoinositide 3- kinase pathyway. Science 2002;296 (5573):1655-1657
[80] Hausenloy DJ, Tsang A, Yellon DM. The reperfusion injury salvage kinase path way: a common target for both ischemic preconditioning and post- conditioning. Trends Cardiovasc 2005;15:69-75
[81] Solenkova NV, Solodushko V, Cohen MV, et al. Endogenous adenosine protects preconditioned heart during early minutes of reperfusion by activating Akt. Am J Physiol Heart Circ Physiol 2006;290:H441-449
[82] Tsang A, Hausenloy DJ, Mocanu MM, et al. Postconditioning: a form of "modified reperfusion" protects the myocardium byactivating the phosphate-dylinositol 3-kinase-Akt pathway. Circ Res 2004;95:230-2
[83] Yang XM, Philipp S, Downey JM, et al. Postconditioning's protection is not dependent on circulating blood factors or cells but involves adenosine receptors and requires PI3-kinase and guanylyl cyclase activation. Basic Res Cardiol 2005;100:57-63
[84] Schwartz LM, Lagranha CJ. Ischemic postconditioning during reperfusion activates Akt and ERK without protecting against lethal myocardial ischemia- reperfusion injury in pigs. Am J Physiol Heart Circ Physiol 2006;290:H1011-H1018
[85] Darling CE, Jiang R, Maynard M, et al. Postconditioning via stuttering reperfusion limits myocardial infarct size in rabbit hearts: role of ERK1/2. Am J Physiol Heart Circ Physiol 2005;289:H1618-H1626
[86] Sun HY, Wang NP, Halkos M, et al. Postconditioning attenuates cardiomyo-cyte apoptosis via inhibition of JNK and p38 mitogen-activated protein kinase signaling pathways. Apoptosis 2006; 11:1583-1593
[87] Bullard AJ, Govewalla P, Yellon DM. Erythropoietin protects the myocardium against reperfusion injury in vitro and in vivo. Basic Res Cardiol 2005; 100:397-403
[88] Hamid SA, Baxter GF. Adrenomedullin limits reperfusion injury in experiment tal myocardial infarction. Basic Res Cardiol 2005; 100:387-396
[89] Smith CC, Mocanu MM, Davidson SM, et al. Leptin, the obesity-associated hormone, exhibits direct cardioprotective effects. Br J Pharmacol 2006; 149:5-13
[90] Ming XF, Viswambharan H, Barandier C, et al. Rho GTPase/Rho kinase negatively regulates endothelial nitric oxide synthase phosphorylation through the inhibition of protein kinase B/Akt in human endothelial cells. Mol Cell Biol 2002;22:8467-8477
[91] Hamid SA, Bower HS, Baxter GF: Rho kinase activation plays a major role as a mediator of irreversible injury in reperfused myocardium. Am J Physiol Heart Circ Physiol 2007;292:H2598-2606
[92] Zatta AJ, Kin H, Lee G, et al. Infarct-sparing effect of myocardial postcondi-tioning is dependent on protein kinase C signalling. Cardiovasc Res 2006;70:315-324
[93] Inagaki K, Begley R, Ikeno F, et al. Cardioprotection by e-protein kinase C activation from ischemia continuous delivery and antiarrhythmic effect of an e-protein kinase C-activating peptide. Circulation 2005; 111:44-50
[94] Inagaki K, Hahn HS, Dorn II GW, et al. Additive protection of the ischemic heart ex vivo by combined treatment with 5-protein kinase C inhibitor and e-protein kinase C activator. Circulation 2003; 108:869-75
[95] M Crompton, A Costi, L Hayat. Evidence for the presence of a reversible Ca~(2+) dependent pore activated by oxidative stress in heart mitochondria. Biochem J 1987;245:915-918
[96] M Crompton. The mitochondrial permeability transition pore and its role in cell death. Biochem J 1999;341:233-249
[97] AP Halestrap, SJ Clarke, SA Javadov. Mitochondrial permeability transition pore opening during myocardial reperfusion — a target for cardioprotection. Cardiovasc Res 2004;61:372-385
[98] AP Halestrap. Calcium, mitochondria and reperfusion injury: a pore way to die.Biochem Soc Trans 2006;34:232-237
[99] F DiLisa, P Bernardi. Mitochondria and ischemia-reperfusion injury of the heart: fixing a hole. Cardiovasc Res 2006;70:191-199
[100] AP Halestrap, PM Kerr, S Javadov, et al. Elucidating the molecular mechanism of the permeability transition pore and its role in reperfusion injury of the heart. Biochim Biophys Acta 1998; 1366:79-94
[101] AP Halestrap. The nature of the stimulation of the respiratory chain of rat liver mitochondria by glucagon pretreatment of animals. Biochem J 1982;204:37-47
[102] V Petronilli, A Nicolli, P Costantini, et al. Regulation of the permeability transition pore, a voltage-dependent mitochondrial channel inhibited by cyclosporin A. Biochim Biophys Acta 1994; 1187:255-259
[103] M Crompton, E Barksby, N Johnson, et al. Mitochondrial intermembrane junctional complexes and their involvement in cell death. Biochimie 2002;84:143-152
[104] JC Martinou, DR Green. Breaking the mitochondrial barrier. Nat Rev Mol Cell Biol 2001;2:63-67
[105] DR Green, G Kroemer, The pathophysiology of mitochondrial cell death.Science 2004;305:626-629
[106] AW Leung, AP Halestrap. Recent progress in elucidating the molecular mechanism of the mitochondrial permeability transition pore. Biochim Biophys Acta 2008; 1777:946-952
[107] Wang C ,Neff D A , Kroilkowski J G ,et al .The influence B-cell lymphoma 2 prorein an antiapoptotic regulator of mitochondria permeability transition, on isoflurane-induced and ischemic postconditioning in rabbits. Anesth Analg 2006,102(5):1355-1360
[108] AP Halestrap, C Brenner. The adenine nucleotide translocase: a central component of the mitochondrial permeability transition pore and key player in cell death. Curr Med Chem 2003;10:1507-1525
[109]Liu XH,Zhang ZY,Sun S,et al.Ischemic postconditioning protects myocardium from ischemia/reperfusion injury through attenuating endoplasmic reticulum stress.Shock 2008;30:422-427
[110]Gumina RJ,Buerger E,Eickmeier C,et al.Inhibition of the Na~+/H~+exchanger confers greater cardioprotection against 90 min of myocardial ischemia than ischemic preconditioning in dogs.Circulation 1999;100:2519-2526 discussion 2469-2572
[111]Fujita M,Asanuma H,Hirata A,et al.Prolonged transient acidosis during early reperfusion contributes to the cardioprotective effects of post-conditioning.Am J Physiol Heart Circ Physiol 2007;292:H2004-2008
[112]姚树桐,刘秀华,王家富.缺血后处理的心肌保护机制研究进展.微循环学杂志 2008;18(1):49-52
[113]杨简,杨俊,丁家望,等.腺苷介导大鼠心脏缺血后适应的保护效应.中华老年心脑血管病杂志 2008;10(4):293-296
[114]Feng J,Lucchinetti E,Ahuja P,et al.Isoflurane postconditioning prevents opening of the mitochondrial permeability transition pore through inhibition of glycogen synthase kinase 3h.Anesthesiology 2005;103:987-95
[115]Obal D,Dettwiler S,Favoccia C,et al.The influence of mitochondrial K_(ATP)-channels in the cardioprotection of preconditioning and postconditioning by sevoflurance in the rat in vivo.Anesth Analg 2005;101:1252-60
[116]Chen ZL,Li TZ,Zhang BX.Morphine Postconditioning protects against reper-fusion injury in the isolated rat hearts.J of Surg Res 2008;145:287-294
[117]Staat P,Rioufol G,Piot C,et al.Postconditioning the human heart.Circulation 2005;112(October):2143-8
[118]Laskey WK.Brief repetitive balloon occlusions enhance reperfusion during percutaneous coronary intervention for acute myocardial infarction:a pilot study.Catheter Cardiovas Interv 2005;65:361-7
[119]Luo W,Li B,Chen R,et al.Effect of ischemic postonditioning in adult valve replacement.Eur J Cardiothorac Surg 2008 Feb;33(2):203-8
[120]Luo W,Li B,Lin G,et al.Postonditioning in cardiac surgery for tetralogy of Fallot. J Thorac Cardiovasc Surg 2007 May; 133(5): 1373-4
[121] Mahaffey KW, Puma JA, Barbagelata NA, et al. Adenosine as an adjunct to thrombolytic therapy for acute myocardial infarction: results of a multicenter, randomized, placebo-controlledtrial: the Acute Myocardial Infarction STudy of ADenosine(AMISTAD) trial. J Am Coll Cardiol 1999;34:1711-20
[122] Quintana JE, Hjemdahl P, Sollevi A, et al. Left ventricular function and cardio vascular events following adjuvant therapy with adenosine in acute myocardial infarction treatedwith thrombolysis, results of the ATTenuation by Adenosine of Cardiac Complications (ATTACC) study. Eur J Clin Pharmacol 2003;59:l-9
[123] Ross AM, Gibbons RJ, Stone GW, et al. A randomized, double-blinded placebo-controlled, multicenter trial of adenosine as an adjunct to reperfusion in the treat- ment of acute myocardial infarction (AMISTAD-Ⅱ). J Am Coll Cardiol 2005;45: 1775-80
[124] Kloner RA, Forman MB, Gibbons RJ, et al. Impact of time to therapy and reperfusion modality on the efficacy of adenosine in acute myocardial infarction: the AMISTAD-2 trial. Eur Heart J 2006;20:2400-5
[125] Andrew P Halestrap, Philippe Pasdois. The role of the mitochondrial permeability transition pore in heart disease. Biochim Biophys Acta 2009; (In Press)
[2] Taylor DO, Edwards LB, Boucek MM, et al. Registry of the International Society for Heart and Lung Transplantation: twenty-fourth official adult heart transplant report 2007. J Heart Lung Transplant 2007;26:769-81
[3] Evers KA, Lewis DD. Estimating the non-heart-beating donor potential at a trauma center. J Transpl Coord 1999;9:186
[4] del Rio Gallegos F, Nunez Pena JR, Soria Garcia A, et al. Non heart beating donors. Successfully expanding the donor's pool. Ann Transplant 2004;9:19
[5] Sanchez-Fructuoso Al, Prats D, Torrente J, et al. Renal transplantation from non-heart-beating donors: a promising alternative to enlarge the donor pool. J Am SocNephrol 2000;11:350
[6] Ad Hoc Committee of the Harvard Medical School to Examine the Definition of Brain Death: A definition of irreversible coma. Report of the Ad Hoc Committee of the Harvard Medical School to Examine the Definition of Brain Death. JAMA 1968;205:337
[7] Belzer FO, Salvatierra 0 Jr. The organization of an effective cadaver renal transplantation program. Transplant Proc 1974;6:93
[8] Calne RY, Loughridge L, MacGillivray JB, et al. Further observations on renal transplants in man from cadaveric donors. Brit Med J 1966;2:1345
[9] Mowbray JF, Cohen SL, Doak PB, et al. Human cadaveric renal transplantation:Report of twenty cases. Br Med J 1965;2:1387
[10] Pletka P, Cohen SL, Hulme B, et al. Cadaveric renal transplantation: An analysis of 165 cases. Lancet 1969;1:1
[11] Hall CL, SansomJR, Obeid M, et al. Agonal phase, ischemic times, and renal vascular abnormalities and outcome of cadaver kidney transplants. Br Med J1975;3:667
[12]Marks WH,Wagner D,Pearson TC,et al.Organ donation and utilization,1995-2004:Entering the collaborative era.Am J Transplantation 2006;6:1101
[13]Hattori R,Ono Y,Yoshimura N,et al.Long term outcome of kidney transplant using non-heart-beating donor:Multicenter analysis of factors affecting graft survival.Clinical Transplantation 2003;17:6 518-521
[14]Dubbeld J,Porte R,Hoek v B,et al.non-heart-beating donor liver transplantation:Experience in the netherlands after introdution of restrictive national protocol.Liver Transplantation 2007;13:6 S195
[15]Dark JH.Lung transplantation from the non-heart-beating donor.Transplantation 2008;86(2)200-201
[16]Kootstra G,Daemen JHC,Oomen APA.Categories of non-heart-beating donors.Transplant Proc 1995;27:2893-4
[17]H.Myron Kauffmana,John D Rosendalea,Sarah E Taranto,et al.Non-heart-beating donors(then)and donation after cardiac death(now).Transplant Rev 2007;21:237-248
[18]Begona JA,Gundry SR,Razzouk,et al.Transplantation of hearts after arrest and resuscitation,early and long term results.J Thorac Cardiovasc Surg 1993;106:1196-201
[19]Michael J.Collins,Sina L Moainie,Bartley P Griffith,et al.Preserving and evaluating hearts with ex vivo machine perfusion:an avenue to improve early graft performance and expand the donor pool.Euro J Cardio-thoracic Surg 2008;34:318-325
[20]龚斌,朱家麟,张宝仁,等.窒息死亡尸体心脏移植复苏的实验研究.第二军医大学学报 1999;20(12):1043-1045
[21]Abbott CP,Lindsey ES,Creech O J r,et al.A technique for heart transplantation in the rat.Arch Surg 1964;89:645-652
[22]Ono K,Lindsey ES.Improved technique of heart transplantation in rats.J Thorac Cardiovasc Surg 1969;57(2):225-229
[23]Heron I.A technique for accessory cervical heart transplantation in rabbits and rats.Acta Pathol Microbiol Scand A Pathol 1971;79:366
[24]李志勇,孙建宁,张硕峰.水合氯醛和戊巴比妥钠对SD大鼠麻醉效果的比较.四川动物 2008;2:299-302
[25]程晓峰,景华,胡小南,等.建立大鼠心脏移位移植模型的麻醉选择.医学研究生学报 2005;18(10):958-959
[26]顾晓,赵鸿,古涛.两种大鼠异位心脏移植模型的制备.复旦大学学报:医学版 2007;34(3):572-575
[27]叶文学,沈振亚,张胜超.高复跳率小鼠颈部异位心脏移植模型的建立.实验动物与比较医学 2008,28(3):148-150
[28]尤颢,廖崇先,赵霞,等.大鼠异位心脏移植模型手术的改良.兰州大学学报:医学版 2008,34(3):9-11
[29]Xiu DR,Uchida H,To H,et al.Simplified method of heterotopic rat heart trans-plantation using the cuff technique:Application to sub lethal dose protocol of methotrexate on allograft survival.Microsurgery 2001;21(1):16-21
[30]苏刚,孙宗全,董念国,等.袖套法小鼠颈部异位心脏移植模型的建立.新乡医学院学报 2006;23(5):534-734
[31]Zhao ZQ,Corvera JS,Halkos ME,et al.Inhibition of myocardial injury by ischemic postconditioning during reperfusion:comparison with ischemic preconditioning.Am J Heart Circ Physiol 2003;285:H579-H588
[32]Kin H,Zhao ZQ,Sun HY,et al.Postconditioning attenuates myocardial ischemia reperfusion injury by inhibiting events in the early minutes of reperfusion.Cardiovasc Res 2004;62:74-85
[33]Yang XM,Proctor JB,Cui L,et al.Multiple,brief coronary occlusions during early reperfusion protect rabbit hearts by targeting cell signaling pathways.J Am Coll Cardiol 2004;44(5):1103-1110
[34]Iliodromitis EK,Georgiadis M,Cohen MV,et al.Protection from postconditioning depends on the number of short ischemic insults in anesthetized pigs.Basic Res Cardiol 2006;101:502-507
[35]Bopassa JC,Ferrera R,Gateau Roesch O,et al.PI-3 kinase regulates the mitochondrial transition pore in controlled reperfusion and postconditioning.Cardiovasc Res 2006;69:178-185
[36]Staat P,Rioufol G,Piot C,et al.Postconditioning the human heart.Circulation 2005;112:2143-8
[37]Laskey WK.Brief repetitive balloon occlusions enhance reperfusion during percutaneous coronary intervention for acute myocardial infarction:a pilot study.Catheter Cardiovas Interv 2005;65:361-7
[38]Luo W,Li B,Chen R,et al.Effect of ischemic postonditioning in adult valve replacement.Eur J Cardiothorac Surg 2008 Feb;33(2):203-8
[39]Glanemann M,Langrehr JM,Stange B J,et al.Clinical implications of hepatic preservation injury after adult liver transplantation.Am J Transplant 2003;3:1003-9
[40]Mueller AR,Platz KP,Haak M,et al.The release of cytokines,adhesion molecules,and extracellular matrix parameters during and after reperfusion in human liver transplantation.Transplantation 1996;62:1118-26
[41]Murry CE,Jenningsx CE,Reimer KA.Preconditioning with ischemia:a delay of lethal cell injury in ischemic myocardium.Circulation 1986;74:1124-36
[42]Landymore RW,Bayes A J,Murphy JT,et al.Preconditioning prevents myocardial stunning after cardiac transplantation.Ann Thorac Surg 1998;66:1953-7
[43]Jassem W,Fuggle SV,Cerundolo L,et al.Ischemic preconditioning of cadaver donor livers protects allografts following transplantation.Transplantation 2006;81:169-74
[44]牛英,叶启发.缺血后处理及其在器官移植术中的应用.中南大学学报(医学版)2008;33(6):548-552
[45]马兰,李力兵,高长青,等.离体供心保存技术的研究现状.中国体外循环杂志 2008;6(4)255-256
[46]Ambrosio G,Zweier JL,Flaherty JT.The relationship between oxygen radical generation and impairment of myocardial energy metabolism following postischemic reperfusion.J Mol Cell Cardiol 1991;23:1359-1374
[47]Kevin LG,Camara AKS,Riess ML,et al.Ischemic preconditioning alters realtime measure of O_2 radicals in intact hearts with ischemia and reperfusion.Am J Physiol(Heart Circ Physiol)2003;284:H566-H574
[48]Scholz W,Albus U,Linz W,et al.Effect of Na~+/H~+exchange inhibitors in cardiac ischemia.J Mol Cell Cardiol 1992;24:731-740
[49]Jordan JE,Zhao ZQ,Vinten-Johansen J.The role of neutrophils in myocardial ischemia-reperfusion injury.Cardiovasc Res 1999;43:860-878
[50]Lefer AM,Tsao PS,Lefer DJ,et al.Role of endothelial dysfunction in the pathogenesis of reperfusion injury after myocardial ischemia.FASEB J 1991;5:2029-2034
[51]Sun HY,Wang NP,Kerendi F,et al.Hypoxic postconditioning reduces cardiomyocyte loss by inhibiting ROS generation and intracellular Ca~(2+)overload.Am J Physiol 2005;288:H1900-H1908
[52]Fujita M,Asanuma H,Hirata A,et al.Prolonged transient acidosis during early reperfusion contributes to the cardioprotective effects of postconditioning.Am J Physiol Heart Circ Physiol 2007;292(4):2004-2008
[53]姚树桐,李玉珍,刘秀华,等.缺血后处理对小肠缺血再灌注损伤大鼠肠系膜微循环的影响.微循环学杂志 2007;17(2):1-4
[54]郭晓笋,刘秀华,张振英,等.缺血后处理通过改善微循环减轻大鼠骨骼肌缺血再灌注损伤.微循环学杂志 2007;17(4):8-11
[55]Zhao ZQ,Sun HY,Wang NP,et al.Hypoxic postconditioning attenuates cardiomyocyte apoptosis via inhibition ofjnk and p38 kinases pathway.J Mol Cell Cardiol 2005;38:870
[56]Andrew P Halestrap,Philippe Pasdois.The role of the mitochondrial permeability transition pore in heart disease.Biochim Biophys Acta 2009;(In Press)
[57]Hall G,Hasday JD,Rogers TB.Regulating the regulator:NF-kappa B signaling in the heart.J Mol Cell Cardiol 2006;41:580-91
[58]Jones WK,Brown M,Wilhide M,et al.NF-kappa B in cardiovascular disease:diverse and specific effects of a“general”transcription factor? Cardio vasc Toxicol 2005;5:183-202
[59]Valen G,Yan ZQ,Hansson GK.Nuclear factor kappa-B and the heart.J Am Coll Cardiol 2001;38:307-14
[60]Chandrasekar B,Freeman GL.Induction of nuclear factor kappa B and active- tion protein 1 in postischemic myocardium. FEBS Lett 1997;401:30-4
[61] Li C, Browder W, Kao RL. Early activation of transcription factor NF kappa B during ischemia in perfused rat heart. Am J Physiol 1999;276:H543-52
[62] Li C, Kao RL, Ha T, et al. Early activation of IKKbeta during in vivo myocardial ischemia. Am J Physiol 2001;280:H1264-71
[63] Zhang C. The role of inflammatory cytokines in endothelial dysfunction. Basic Res Cardiol 2008;103(5):398-406
[64] Dorge H, Schulz R, Belosjorow S, et al. Coronary microembolization: the role of TNF-alpha in contractile dysfunction. J Mol Cell Cardiol 2002;34(l):51-62
[65] Schulz R, Aker S, Belosjorow S, et al. TNF alpha in ischemia/reperfusion injury and heart failure. Basic Res Cardiol 2004;99(1):8-11
[66] Chandra J, Samali A, Orrenius S. Triggering and modulation of apoptosis by oxidative stress. Free Radic Biol Med 2000;29:323
[67] Yang S, Zheng R, Hu S, et al. Mechanism of cardiac depression after trauma-hemorrhage: increased cardiomyocyte IL-6 and effect of sex steroids on IL-6 regulation and cardiac function. Am J Physiol: Heart Circ Physiol 2004; 287:H2183-91
[68] Ikeda U, Ohkawa F, Seino Y, et al. Serum interleukin 6 levels become elevated in acute myocardial infarction. J Mol Cell Cardiol 1992;24:579-84
[69] Kin H, Wang NP, Mykytenko J, et al. Inhibition of myocardial apoptosis by postconditioning is associated with attenuation of oxidative stress-mediated nuclear factor-kappa B translocation and TNF alpha release. Shock 2008 Jun;29(6):761 -8
[70] Fliss H, Gattinger D. Apoptosis in ischemic and reperfused rat myocardium.Circ Res 1996;79(5):949
[71] Inserte J, Tairmor G, Hof staetter B, et al. Influence of simulated ischemia on apoptosis induction by oxidative stress in adult cardiomyocytes of rats. Am J Physiol Heart Circ Physiol 2000;278(1):94-99
[72] JS Kim, Y Jin, JJ Lemasters. Reactive oxygen species, but not Ca~(2+) over loading, trigger pH and mitochondrial permeability transition-dependent death of adult rat myocytes after ischemia-reperfusion.Am J Physiol 2006;290:H2024-H2034
[73]Kim JS,He L,Lemasters JJ.Mitochondrial permeability transition:a common pathway to necrosis and apoptosis.Biochem Biophys Res Commun 2003;304:463-470
[74]姚树桐,刘秀华,王家富.缺血后处理的心肌保护机制研究进展.微循环学杂志 2008;18(1):49-52
[75]Knudson CM,Korsmeyer SJ.Bcl-2 and bax function independently to regulate cell death.Nat Genet 1997;16(4):358
[76]Antonsson B,Conti F,Ciavat ta A,et al.Inhibition of bax channel forming activity by bcl-2.Science 1997;277(5324):370
[77]Naumovski L,Cleary ML.The p53-binding 53 BP2 also interacts with bcl-2and impedes cell cycle progression at G2/M.Mol Cell Biol 1996;16:3884
[78]Adams JM,Cory S.Life-or-death decisions by the Bcl-2 protein family.Trends Biochem Sci 2001;26:61-66
[79]吴青,陶宏凯,陶大昌,等.灌注诱导心肌细胞凋亡及凋亡相关基因表达的研究.中国心血管病研究杂志 2004;2(11):905
[80]Borutaite V,Brown GC.Mitochondria in apoptosis of ischemic heart.FEBS Lett 2003;541(123):1
[81]Dwaine S Burley,Gary F Baxter.Pharmacological targets revealed by myocardial postconditioning.Curr Opin Pharmacol 2008;Dec:(In Press)
[82]Pitarys C J,Virmani R,Vildibill HD Jr,et al.Reduction of myocardial reperfusion injury by intravenous adenosine administered during the early reperfusion period.Circulation 1991;83:237-247
[83]Kin H,Lofye MT,Amerson BS,et al.Cardioprotection by“postconditioning” is mediated by increased retention of endogenous intravascular adenosine and activationof A_(2a)receptors during reperfusion.Circulation 2004;110:Ⅲ-168
[84]Fryer RM,Auchampach JA,Gross GJ.Therapeutic receptor targets of ischemic preconditioning.Cardiovasc Res 2002;55:520-5
[85]Michael V Cohen,James M Downey.Adenosine at reperfusion:A conundrum ready to be resolved. J Am Coll Cardiol 2009 Feb 24;53(8):718-9
[86] Schulte G, Fredholm BB. Signalling from adenosine receptors to mitogen-activateed protein kinases. Cell Signal 2003; 15:813-827
[87] Mubagwa K, Flameng W. Adenosine, adenosine receptors and myocardial protection: an updated overview. Cardiovasc Res 2001 ;52:25-39
[88] Jason N Peart, John P Headrick. Adenosinergic cardioprotection: Multiple receptors, multiple pathways. Pharmaco Ther 2007; 114:208-221
[89] Kilpatrick EL, Narayan P, Mentzer RM Jr, et al. Cardiacmyocyte adenosine A2a receptor activation fails to alter cAMP or contractility: role of receptor localization. Am J Physiol 2002;282:H1035-H1040
[90] David Ribe, David Sawbridge, Sapna Thakur, et al. Adenosine A_(2A) receptor signaling regulation of cardiac NADPH oxidase activity. Free Radic Biol Med 2008;44:1433-1442
[91] Nolte D, Lorenzen A, Lehr HA, et al. Reduction of postischemic leukocyte endothelium interaction by adenosine via A2 receptor. Naunyn Schmiedebergs Arch Pharmacol 1992;346:234-7
[92] Zhao ZQ, Sato H, Williams MW, et al. Adenosine A2-receptor activation inhibits neutrophil-mediated injury to coronary endothelium. Am J Physiol 1996;271:H1456-64
[93] Aleksander Jovanovic', Alexey E Alekseev, Jo'se R Lo' pez, et al. Adenosine prevents hyperkalemia-induced calcium loading in cardiac cells: Relevance for cardioplegia. Ann Thorac Surg 1997;63:153-61
[94] Zhao ZQ, Budde J M., Morris C D, et al. Adenosine attenuates reperfusion-induced apoptotic cell death by modulating expression of Bcl-2 and Bax proteins. J Mol Cell Cardiol 2001;33:57-68
[95] Yang XM, Philipp S, Downey JM, et al. Postconditioning's protection is not dependent on circulating blood factors or cells but involves adenosine receptors and requires PI3-kinase and guanylyl cyclase activation. Basic Res Cardiol 2005;100:57-63
[96] Kin H, Zatta AJ, Lofye MT, et al. Postconditioning reduces infarct size via adenosine receptor activation by endogenous adenosine.Cardiovasc Res 2005;67:124-133
[97]Philipp S,Yang XM,Cui L,et al.Postconditioning protects rabbit hearts through a protein kinase C-adenosine A2b receptor cascade.Cardiovasc Res 2006;70:308-314
[98]Takahama H,Minamino T,Asanuma H,et al.Prolonged targeting of ischemic/reperfused myocardium by liposomal adenosine augments cardioprotection in rats.J Am Coll Cardiol 2009;53:709-17
[99]Pitarys CJ Ⅱ,Virmani R,Vildibill HD Jr,et al.Reduction of myocardial reperfusion injury by intravenous adenosine administered during the early reperfusion period.Circulation 1991;83:237-47
[100]Jason M Budde,Cullen D Morris,Daniel A Velez,et al.Reduction of infarct size and preservation of endothelial function by multidose intravenous adenosine during extended reperfusion.J Surg Res 2004;116,104-115
[101]Goto M,Miura T,Iliodoromitis EK,et al.Adenosine infusion during early reperfusion failed to limit myocardial infarct size in a collateral deficient species.Cardiovasc Res 1991;25:943-9
[102]Claudia Penna,Daniele Mancardi,Francesca Tullio,et al.Intermittent adenosine at the beginning of reperfusion does not trigger cardioprotection.J Surg Res 2008;(In Press)
[103]Thourani VH,Ronson RS,Van Wylen DG,et al.Adenosine-supplemented blood cardioplegia attenuates postischemic dysfunction after severe regional ischemia.Circulation 1999;100:Ⅱ376-83
[104]李芝,邵永丰,梁永,等.腺苷在心脏直视术中心肌保护作用的研究.中国体外循环杂志 2008;6(3):149-151
[105](?)yvind Jakobsen,Stig Muller,Erling Aarsaether,et al.Adenosine instead of supranormal potassium in cardioplegic solution improves cardioprotection.Eur J Cardiothorac Surg 2007;32:493-500
[1] Jennings RB, Sommer HM, Smyth GA, et al. Myocardial necrosis induced by temporary occlusion of a coronary artery in the dog. Arch Pathol 1960;70:68-78
[2] Goldhaber JI, Weiss JN. Oxygen free radicals and cardiac reperfusion abnormalities. Hypertension 1992;20:l 18-127
[3] Jacob Vinten-Johansen. Postconditioning: a mechanical maneuver that triggers biological and molecular cardioprotective responses to reperfusion. Heart Fail Rev 2007; 12:235-244
[4] Becker LC, Ambrosio G. Myocardial consequences of reperfusion. Prog Cardio vasc Dis 1987;30:23-44
[5] Forman MB, Virmani R, Puett DW. Mechanisms and therapy of myocardial reperfusion injury. Circulation 1990;81(suppl Ⅳ):Ⅳ-69-78
[6] Hearse DJ, Bolli R. Reperfusion induced injury: manifestations, mechanisms,and clinical relevance. [Review]. Cardiovasc Res 1992;26:101-8
[7] Jeroudi MO, Hartley CJ, Bolli R. Myocardial reperfusion injury: role of oxygen radicals and potential therapy with antioxidants. [Review]. Am J Cardiol 1994;73:2B-7B
[8] Jordan JE, Zhao ZQ, Vinten-Johansen J. The role of neutrophils in myocardial ischemia-reperfusion injury. Cardiovasc Res 1999;43: 860-78
[9] Lucchesi BR. Complement, neutrophils and free radicals: mediators of reperfusion injury. [Review]. Arzneim-Forsch/Drug Res 1994;44:420-32
[10] Opie LH. Role of calcium and other ions in reperfusion injury. Cardiovasc Drugs Ther 1991;5:237-47
[11] Piper HM, Meuter K, Schafer C. Cellular mechanisms of ischemia-reperfusion injury. Ann Thorac Surg 2003;75:S644-8
[12] Jean Pierre Monassier. Reperfusion jnjury in acute myocardial infarction: From bench to Cath lab. Part I : Basic considerations. Arch Cardiovas Dis 2008;101(7-8):491-500
[13] Murry CE, Jennings RB, Reimer KA. Preconditioning with ischemia: A delay of lethal cell injury in ischemic myocardium. Circulation 1986;74:1124-1136
[14] Zhao ZQ, Corvera JS, Halkos ME, et al. Inhibition of myocardical injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. Am J Heart Circ Physiol 2003;285:H579-H588
[15] Kin H, Zhao ZQ, Sun HY, et al. Postconditioning attenuates myocardial ischemia-reperfusion injury by inhibiting events in the early minutes of reperfusion. Cardiovasc Res 2004;62:74-85
[16] Yang XM, Proctor JB, Cui L, et al. Multiple, brief coronary occlusions during early reperfusion protect rabbit hearts by targeting cell signaling pathways. J Am Coll Cardiol 2004;44(5):1103-1110
[17] Iliodromitis EK, Georgiadis M, Cohen MV, et al. Protection from postconditioning depends on the number of short ischemic insults in anesthetized pigs.Basic Res Cardiol 2006; 101:502-507
[18] Bopassa JC, Ferrera R, Gateau Roesch O, et al. PI-3 kinase regulates the mitochondrial transition pore in controlled reperfusion and postconditioning. Cardiovasc Res 2006;69:178-185
[19] Sun HY, Wang NP, Kerendi F, et al. Hypoxic postconditioning reduces cardio-myocyte loss by inhibiting ROS generation and intracellular Ca~(2+) overload. Am J Physiol 2005;288:H1900-8
[20] K Sun, ZS Liu, Q Sun. Role of mitochondria in cell apoptosis during hepatic ischemia-reperfusion injury and protective effect of ischemic postconditioning. World J Gastroenterol 2004; 10:1934-1938
[21] Eldaif SM, Geneve J, Wang NP, et al. Postconditioning beyond the heart: Post conditioning the ischemic kidney attentutes renal reperfusion injury. Circulation 2007; 116(16) :61-62
[22] H Zhao, RM Sapolsky, GK Steinberg. Interrupting reperfusion as a stroke therapy: ischemic postconditioning reduces infarct size after focal ischemia in rats. J Cereb Blood Flow Metab 2006;26:1114-1121
[23] dos Santos CHM, Gomes OM, Pontes JCDV, et al. The ischemic preconditioning and postconditioning effect on the intestinal mucosa of rats undergoing the ot mesenteric ischemia/reperfusion procedure.Acta Cirugica Brasileira 2008;23:22-28
[24]Wu XD,Zhang ZY,Liu XH,et al.Ischemic postconditioning protects skeletal muscle from reperfusion injury through calreticulin regulated.J of Amer Colle of Cadio 2008;51-10:B75
[25]Kerendi F,Kin H,Halkos ME,et al.Remote postconditioning.Brief renal ischemia and reperfusion applied before coronary artery reperfusion reduces myocard ial infarct size via endogenous activation of adenosine receptors.Basic Res Cardiol 2005;100:404-12
[26]袁志柳,刘兴德,陈保林等.缺血后处理对缺血再灌注大鼠心肌梗死面积、CK、MDA及SOD的影响.微循环学杂志 2006;16:27-28,31
[27]杨国杰,李运伟,曾秋棠等.缺血后处理对兔缺血再灌注心肌细胞凋亡及Bcl -2和Bax蛋白表达的影响.郑州大学学报(医学版)2008;43:57-59
[28]郭晓笋,刘秀华,张振英等.缺血后处理通过改善微循环减轻大鼠骨骼肌缺血再灌注损伤.微循环学杂志 2007;17(4):8-11.
[29]郑鸣之,蒋建平,陈莹莹等.缺血后处理对不同时程冷保存大鼠心脏的作用研究.浙江大学学报(医学版)2007;36(6):567-574
[30]Galagudza M,Kurapeev D,Minasian S,et al.Ischemic postconditioning:brief ischemia during reperfusion converts persistent ventricular fibrillation into regular rhythm.Eur J Cardio-Thorac Surg 2004;25:1006-10
[31]Desagher S,Martinou JC.Mitochondria as the central contral point of apoptosis.Trends Cell Biol 2000;10(9):369-377
[32]Zhao ZQ,Sun HY,Wang NP,et al.Hypoxic postconditioning attenuates cardio myocyte apoptosis via inhibition ofjnk and p38 kinases pathway.J Mol Cell Cardiol 2005;38:870
[33]Philipp SD,Downey JM,Cohen MV.Postconditioning must be initiated in less than l minute following reperfusion and is dependent on adenosine receptors and P13-kinase.Circulation 2004;110:Ⅲ-168
[34]Burda J,Danielisova V,Nemethova,M,et al.Delayed postconditionig initiates additive mechanism necessary for survival of selectively vulnerable neurons after transient ischemia in rat brain. Cell Mol Neurobiol 2006;26(7-8): 1141-1151
[35] Zhao ZQ, Jakob Vinten-Johansen. Postconditioning: Reduction of reperfusion induced injury. Cardiovasc Res 2006;70:200-211
[36] Mykytenko J, Kerendi F, Reeves JG, et al. Long-term inhibition of myocardial infarction by postconditioning during reperfusion. Basic Res Cardiol 2007; 102:90-100.
[37] Mykytenko J, Reeves JG, Kin H, et al. Postconditioning reduces infarct size via mitochondrial K_(Atp) channel activation during 24 hours of reperfusion. J Mol Cell Cardiol 2005;38:830
[38] Andreka G, Vertesaljai M, Szantho G, et al. Remote ischemic postconditioning protects the heart during acute myocardial infarction of pigs. Heart 2007; 93:749-752
[39] Argaud L, Gateau-Roesch O, Raisky O, et al. Post conditioning inhibits mitochondrial permeability transition. Circulation 2005; 111:194-197
[40] Vinten-Johansen Jakob, Kin Hajime, Sun He Ying, et al. Postconditioning reduces myocardial injury by inhibiting reactive oxygen species during reperfusion. Circulation 2003; 108(17): Ⅳ-219
[41] Engelman DT, Watanabe M, Engleman RM, et al. Constitutive nitric oxide release is impaired after ischemia and reperfusion. J Thorac Cardiovasc Surg1995;110:1047-53
[42] Ma X-L, Weyrich AS, Lefer DJ, et al. Diminished basal nitric oxide release after myocardial ischemia and reperfusion promotes neutrophil adherence to coronary endothelium. Circ Res 1993;72:403-12
[43] Palazzo AJ, Jones SP, Anderson DC, et al. Coronary endothelial P-selectin in pathogenesis of myocardial ischemia injury. Am J Physiol (Heart Circ Physiol) 1998;275:H1865-72
[44] Weyrich AS, Ma X-L, Lefer DJ, et al. In vivo neutralization of P-selectin protects feline heart and endothelium in myocardial ischemia and reperfusion injury.J Clin Invest 1993;91:2620-9
[45]Scholz W,Albus U,Linz W,et al.Effect of Na~+/H~+exchange inhibitors in cardiac ischemia.J Mol Cell Cardiol 1992;24:731-740
[46]姚树桐,李玉珍,刘秀华,等.缺血后处理对小肠缺血再灌注损伤大鼠肠系膜微循环的影响.微循环学杂志2007;17(2):1-4
[47]Keith A Webster.Programmed death as a therapeutic target to reduce myocardial infarction.Trends Pharmacol Sci 2007;28(9):492-499
[48]Yamaguchi H,Wang HG:The protein kinase PKB/Akt regulates cell survival and apoptosis by inhibiting Bax conformational change.Oncogene 2001,20:7779-7786
[49]Cronstein BN,Kramer SB,Weissmann G,et al.Adenosine:a physiological modulator of superoxide anion generation by human neutrophils.J Exp Med 1983;158:1160-77
[50]Kitakaze M,Hori M,Sato H,et al.Endogenous adenosine inhibits platelet aggregation during myocardial ischemia in dogs.Circ Res 1991;69:1402-8
[51]Colli S,Tremoli E.Multiple effects of dipyridamole on neutrophils and mononuclear leukocytes:adenosine dependent and adenosine-independent mechanisms.J Lab Clin Med 1991;118:136-45
[52]Williams MW,Jordan JE,Fernandez AZ,et al.Adenosine(ADO)inhibits unactivated neutrophil(PMN)adherence to thrombin stimulated coronary vascular endothelium(EC)by a p-selectin mechanism.FASEB J 1996;10:280
[53]Cronstein BN,Levin RI,Philips M,et al.Neutrophil adherence to endothelium is enhanced viaadenosine Al receptors and inhibited via adenosine A2receptors.J Immunol 1992;148:2201-6
[54]Nakamura M,Zhao Z-Q,Clark KL,et al.A novel adenosine analog,AMP579,inhibits neutrophil activation,adherence and neutrophil-mediated injury to coronary vascular endothelium.Eur J Pharm 2000;397:197-205
[55]Nolte D,Lehr HA,Messmer K.Adenosine inhibits postischemic leukocyte-endothelium interaction in postcapillary venules of the hamster.Am J Physiol 1991;261:H651-5
[56] Philipp S, Yang XM, Cui L, et al. Postconditioning protects rabbit hearts through a protein kinase C-adenosine A2b receptor cascade. Cardiovasc Res2006;70:308-314
[57] Lefer DJ, Nakanishi K, Vinten-Johansen J, et al. Cardiac venous endothelial dysfunction after myocardial ischemia and reperfusion in dogs. Am J Physiol 1992; 263:H850-6
[58] Tsao PS, Aoki N, Lefer DJ, et al. Time course of endothelial dysfunction and myocardial injury during myocardial ischemia and reperfusion in the cat. Circulation 1990;82:1402-12
[59] Johnson Ⅲ G, Tsao PS, Lefer AM. Cardioprotective effects of authentic nitric oxide in myocardial ischemia with reperfusion. Crit Care Med 1991; 19:244-52
[60] Pagliaro PR, Rastaldo R, Penna C, et al. Nitric oxide (NO)-cyclic guanosine monophosphate (cGMP) pathway is involved in ischemic postconditioning in the isolated rat heart. Circulation 2004; 110:111-136
[61] Ventura C, Bastagli L, Bernardi P, et al. Opioid receptors in rat cardiac sarcolemma: effect of phenylephrine and isoproterenol. Biochim Biophys Acta 1989;987: 69-74
[62] Wittert G, Hope P, Pyle D. Tissue distribution of opioid receptor gene expression in the rat. Biochem Biophys Res Commun 1996;218:877-81
[63] Kin H, Zatta AJ, Jiang R, et al. Activation of opioid receptors mediates the infarct size reduction by postconditioning. J Mol Cell Cardiol 2005;38:827
[64] Bolli R. Oxygen-derived free radicals and myocardial reperfusion injury: an overview. Cardiovasc Drugs Ther 1991;5(Suppl2):249-68
[65] Herkert O, Diebold I, Brandes RP, et al. NADPH oxidase mediates tissue factor-dependent surface procoagulant activity by thrombin in human vascular smooth muscle cells. Circulation 2002; 105:2030-6
[66] Penna C, Rastaldo R, Mancardi D, et al. Post-conditioning induced ardioprotec- tion requires signaling through a redox-sensitive mechanism, mitochondrial ATP sensitive K~+ channel and protein kinase C activation. Bas Res Cardiol 2006 Mar; 101(2): 180-9
[67] Marceau F, Hess JF, Bachvarov DR. The B1 receptors for kinins. Pharmacol Rev 1998;50:357-86
[68] Tschope C, Heringer Walther S, Koch M, et al. Myocardial bradykinin B2 receptor expression at different time points after induction of myocardial infarcttion. J Hyperten 2000; 18:223-8
[69] Bell RM, Yellon DM. Bradykinin limits infarction when administered as an adjunct to reperfusion in mouse heart: the role of PI3K. Akt and eNOS. J Mol CellCardiol2003;35:185-193
[70] Penna C, Mancardi D, Rastaldo R, et al. Intermittent activation of bradykinin B2 receptors and mitochondrial K_(Atp) channels trigger cardiac postcondition- ing through redox signaling. Cardiovasc Res 2007;75:168-177
[71] Penna C, Mancardi D, Tullio F, et al. Postconditioning and intermittent bradykinin induced cardioprotection require cyclooxygenase activation and prostacyclin release during reperfusion. Basic Res Cardiol 2008, 103:368-377
[72] Kis A, Yellon DM, Baxter GF. Role of nuclear factor- _KB activation in acute ischemia-reperfusion injury in myocardium. Br J Pharmacol 2003; 138:894
[73] Cargnoni A, Ceconi C, Gaia G, et al. Cellular thiols redox status: A switch for NF-_kB activation during myocardial post-ischaemic reperfusion. J Mol Cell Cardiol 2002;34:997
[74] M Zhang, YJ Xua, Harjot K, Sainia, et al. TNF-a as a potential mediator of cardiac dysfunction due to intracellular Ca~(2+)-overload. Biochem Biophys Res Commun 2005;327:57-63
[75] Kin H, Wang NP, Mykytenko J, et al. Inhibition of myocardial apoptosis by postconditioning is associated with attenuation of oxidative stress-mediated nuclear factor-kappa B translocation and TNF alpha release. Shock 2008 Jun;29(6):761-8
[76] Jobe LJ, Jiang R, Wang N-P, et al. Tissue factor, factors Ⅶa and Xa expression and local generation of thrombin in at risk myocardium occurs specifically during reperfusion. Circulation 2004;l 10:111-297
[77] Mackman N. The role of the tissue factor-thrombin pathway in cardiac ischemia-reperfusion injury. Semin Vasc Med 2003 ;3:193-8
[78] Jiang R, Reeves JG, Mykytenko J, et al. Postconditioning reduces reperfusion injury by inhibiting the tissue factor-thrombin pathway in a closed-chest porcine modelof ischemia-reperfusion. Circulation 2005;112(Suppl Ⅱ):Ⅱ-309
[79] Cantley LC. The phosphoinositide 3- kinase pathyway. Science 2002;296 (5573):1655-1657
[80] Hausenloy DJ, Tsang A, Yellon DM. The reperfusion injury salvage kinase path way: a common target for both ischemic preconditioning and post- conditioning. Trends Cardiovasc 2005;15:69-75
[81] Solenkova NV, Solodushko V, Cohen MV, et al. Endogenous adenosine protects preconditioned heart during early minutes of reperfusion by activating Akt. Am J Physiol Heart Circ Physiol 2006;290:H441-449
[82] Tsang A, Hausenloy DJ, Mocanu MM, et al. Postconditioning: a form of "modified reperfusion" protects the myocardium byactivating the phosphate-dylinositol 3-kinase-Akt pathway. Circ Res 2004;95:230-2
[83] Yang XM, Philipp S, Downey JM, et al. Postconditioning's protection is not dependent on circulating blood factors or cells but involves adenosine receptors and requires PI3-kinase and guanylyl cyclase activation. Basic Res Cardiol 2005;100:57-63
[84] Schwartz LM, Lagranha CJ. Ischemic postconditioning during reperfusion activates Akt and ERK without protecting against lethal myocardial ischemia- reperfusion injury in pigs. Am J Physiol Heart Circ Physiol 2006;290:H1011-H1018
[85] Darling CE, Jiang R, Maynard M, et al. Postconditioning via stuttering reperfusion limits myocardial infarct size in rabbit hearts: role of ERK1/2. Am J Physiol Heart Circ Physiol 2005;289:H1618-H1626
[86] Sun HY, Wang NP, Halkos M, et al. Postconditioning attenuates cardiomyo-cyte apoptosis via inhibition of JNK and p38 mitogen-activated protein kinase signaling pathways. Apoptosis 2006; 11:1583-1593
[87] Bullard AJ, Govewalla P, Yellon DM. Erythropoietin protects the myocardium against reperfusion injury in vitro and in vivo. Basic Res Cardiol 2005; 100:397-403
[88] Hamid SA, Baxter GF. Adrenomedullin limits reperfusion injury in experiment tal myocardial infarction. Basic Res Cardiol 2005; 100:387-396
[89] Smith CC, Mocanu MM, Davidson SM, et al. Leptin, the obesity-associated hormone, exhibits direct cardioprotective effects. Br J Pharmacol 2006; 149:5-13
[90] Ming XF, Viswambharan H, Barandier C, et al. Rho GTPase/Rho kinase negatively regulates endothelial nitric oxide synthase phosphorylation through the inhibition of protein kinase B/Akt in human endothelial cells. Mol Cell Biol 2002;22:8467-8477
[91] Hamid SA, Bower HS, Baxter GF: Rho kinase activation plays a major role as a mediator of irreversible injury in reperfused myocardium. Am J Physiol Heart Circ Physiol 2007;292:H2598-2606
[92] Zatta AJ, Kin H, Lee G, et al. Infarct-sparing effect of myocardial postcondi-tioning is dependent on protein kinase C signalling. Cardiovasc Res 2006;70:315-324
[93] Inagaki K, Begley R, Ikeno F, et al. Cardioprotection by e-protein kinase C activation from ischemia continuous delivery and antiarrhythmic effect of an e-protein kinase C-activating peptide. Circulation 2005; 111:44-50
[94] Inagaki K, Hahn HS, Dorn II GW, et al. Additive protection of the ischemic heart ex vivo by combined treatment with 5-protein kinase C inhibitor and e-protein kinase C activator. Circulation 2003; 108:869-75
[95] M Crompton, A Costi, L Hayat. Evidence for the presence of a reversible Ca~(2+) dependent pore activated by oxidative stress in heart mitochondria. Biochem J 1987;245:915-918
[96] M Crompton. The mitochondrial permeability transition pore and its role in cell death. Biochem J 1999;341:233-249
[97] AP Halestrap, SJ Clarke, SA Javadov. Mitochondrial permeability transition pore opening during myocardial reperfusion — a target for cardioprotection. Cardiovasc Res 2004;61:372-385
[98] AP Halestrap. Calcium, mitochondria and reperfusion injury: a pore way to die.Biochem Soc Trans 2006;34:232-237
[99] F DiLisa, P Bernardi. Mitochondria and ischemia-reperfusion injury of the heart: fixing a hole. Cardiovasc Res 2006;70:191-199
[100] AP Halestrap, PM Kerr, S Javadov, et al. Elucidating the molecular mechanism of the permeability transition pore and its role in reperfusion injury of the heart. Biochim Biophys Acta 1998; 1366:79-94
[101] AP Halestrap. The nature of the stimulation of the respiratory chain of rat liver mitochondria by glucagon pretreatment of animals. Biochem J 1982;204:37-47
[102] V Petronilli, A Nicolli, P Costantini, et al. Regulation of the permeability transition pore, a voltage-dependent mitochondrial channel inhibited by cyclosporin A. Biochim Biophys Acta 1994; 1187:255-259
[103] M Crompton, E Barksby, N Johnson, et al. Mitochondrial intermembrane junctional complexes and their involvement in cell death. Biochimie 2002;84:143-152
[104] JC Martinou, DR Green. Breaking the mitochondrial barrier. Nat Rev Mol Cell Biol 2001;2:63-67
[105] DR Green, G Kroemer, The pathophysiology of mitochondrial cell death.Science 2004;305:626-629
[106] AW Leung, AP Halestrap. Recent progress in elucidating the molecular mechanism of the mitochondrial permeability transition pore. Biochim Biophys Acta 2008; 1777:946-952
[107] Wang C ,Neff D A , Kroilkowski J G ,et al .The influence B-cell lymphoma 2 prorein an antiapoptotic regulator of mitochondria permeability transition, on isoflurane-induced and ischemic postconditioning in rabbits. Anesth Analg 2006,102(5):1355-1360
[108] AP Halestrap, C Brenner. The adenine nucleotide translocase: a central component of the mitochondrial permeability transition pore and key player in cell death. Curr Med Chem 2003;10:1507-1525
[109]Liu XH,Zhang ZY,Sun S,et al.Ischemic postconditioning protects myocardium from ischemia/reperfusion injury through attenuating endoplasmic reticulum stress.Shock 2008;30:422-427
[110]Gumina RJ,Buerger E,Eickmeier C,et al.Inhibition of the Na~+/H~+exchanger confers greater cardioprotection against 90 min of myocardial ischemia than ischemic preconditioning in dogs.Circulation 1999;100:2519-2526 discussion 2469-2572
[111]Fujita M,Asanuma H,Hirata A,et al.Prolonged transient acidosis during early reperfusion contributes to the cardioprotective effects of post-conditioning.Am J Physiol Heart Circ Physiol 2007;292:H2004-2008
[112]姚树桐,刘秀华,王家富.缺血后处理的心肌保护机制研究进展.微循环学杂志 2008;18(1):49-52
[113]杨简,杨俊,丁家望,等.腺苷介导大鼠心脏缺血后适应的保护效应.中华老年心脑血管病杂志 2008;10(4):293-296
[114]Feng J,Lucchinetti E,Ahuja P,et al.Isoflurane postconditioning prevents opening of the mitochondrial permeability transition pore through inhibition of glycogen synthase kinase 3h.Anesthesiology 2005;103:987-95
[115]Obal D,Dettwiler S,Favoccia C,et al.The influence of mitochondrial K_(ATP)-channels in the cardioprotection of preconditioning and postconditioning by sevoflurance in the rat in vivo.Anesth Analg 2005;101:1252-60
[116]Chen ZL,Li TZ,Zhang BX.Morphine Postconditioning protects against reper-fusion injury in the isolated rat hearts.J of Surg Res 2008;145:287-294
[117]Staat P,Rioufol G,Piot C,et al.Postconditioning the human heart.Circulation 2005;112(October):2143-8
[118]Laskey WK.Brief repetitive balloon occlusions enhance reperfusion during percutaneous coronary intervention for acute myocardial infarction:a pilot study.Catheter Cardiovas Interv 2005;65:361-7
[119]Luo W,Li B,Chen R,et al.Effect of ischemic postonditioning in adult valve replacement.Eur J Cardiothorac Surg 2008 Feb;33(2):203-8
[120]Luo W,Li B,Lin G,et al.Postonditioning in cardiac surgery for tetralogy of Fallot. J Thorac Cardiovasc Surg 2007 May; 133(5): 1373-4
[121] Mahaffey KW, Puma JA, Barbagelata NA, et al. Adenosine as an adjunct to thrombolytic therapy for acute myocardial infarction: results of a multicenter, randomized, placebo-controlledtrial: the Acute Myocardial Infarction STudy of ADenosine(AMISTAD) trial. J Am Coll Cardiol 1999;34:1711-20
[122] Quintana JE, Hjemdahl P, Sollevi A, et al. Left ventricular function and cardio vascular events following adjuvant therapy with adenosine in acute myocardial infarction treatedwith thrombolysis, results of the ATTenuation by Adenosine of Cardiac Complications (ATTACC) study. Eur J Clin Pharmacol 2003;59:l-9
[123] Ross AM, Gibbons RJ, Stone GW, et al. A randomized, double-blinded placebo-controlled, multicenter trial of adenosine as an adjunct to reperfusion in the treat- ment of acute myocardial infarction (AMISTAD-Ⅱ). J Am Coll Cardiol 2005;45: 1775-80
[124] Kloner RA, Forman MB, Gibbons RJ, et al. Impact of time to therapy and reperfusion modality on the efficacy of adenosine in acute myocardial infarction: the AMISTAD-2 trial. Eur Heart J 2006;20:2400-5
[125] Andrew P Halestrap, Philippe Pasdois. The role of the mitochondrial permeability transition pore in heart disease. Biochim Biophys Acta 2009; (In Press)
© 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 |