Prime causes of rapid cardiomyocyte death during reperfusion

被引:83
作者
Piper, HM
García-Dorado, D
机构
[1] Univ Giessen Klinikum, Inst Physiol, D-35392 Giessen, Germany
[2] Hosp Gen Valle Hebron, Serv Cardiol, Barcelona, Spain
关键词
D O I
10.1016/S0003-4975(99)01025-5
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
In ischemic-reperfused myocardium, necrosis of cardiomyocytes may develop not only due to the ischemic conditions but also the specific circumstances of reperfusion. The existence of reperfusion injury becomes apparent when modifications of the conditions of reperfusion can prevent cell death otherwise occurring. Three prime causes of rapidly developing reperfusion injury are here discussed, ie, reenergization of cells at increased cytosolic Ca2+ contents, rapid normalization of tissue pH, and rapid normalization of tissue osmolality. All three causes lead to severe mechanical stress of cardiomyocytes which can cause their rapid deterioration. Propagation of cell injury among adjacent cells can cause a spreading of necrosis throughout myocardial tissue. The understanding of these initial causes of rapidly developing lethal reperfusion injury leads to new concepts for specific protection of reperfused myocardium. (C) 1999 by The Society of Thoracic Surgeons.
引用
收藏
页码:1913 / 1919
页数:7
相关论文
共 25 条
  • [1] DOWNEY JM, 1992, MYOCARDIAL PROTECTION, P35
  • [2] Reperfusion injury: Does it exist and does it have clinical relevance?
    Ferrari R.
    Hearse D.J.
    [J]. Journal of Thrombosis and Thrombolysis, 1997, 4 (1) : 25 - 34
  • [3] GANOTE CE, 1990, PATHOPHYSIOLOGY SEVE, P337
  • [4] GarciaDorado D, 1997, CIRCULATION, V96, P3579
  • [5] FAVORABLE EFFECTS OF HYPEROSMOTIC REPERFUSION ON MYOCARDIAL EDEMA AND INFARCT SIZE
    GARCIADORADO, D
    THEROUX, P
    MUNOZ, R
    ALONSO, J
    ELIZAGA, J
    FERNANDEZAVILES, F
    BOTAS, J
    SOLARES, J
    SORIANO, J
    DURAN, JM
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY, 1992, 262 (01): : H17 - H22
  • [6] SELECTIVE-INHIBITION OF THE CONTRACTILE APPARATUS - A NEW APPROACH TO MODIFICATION OF INFARCT SIZE, INFARCT COMPOSITION, AND INFARCT GEOMETRY DURING CORONARY-ARTERY OCCLUSION AND REPERFUSION
    GARCIADORADO, D
    THEROUX, P
    DURAN, JM
    SOLARES, J
    ALONSO, J
    SANZ, E
    MUNOZ, R
    ELIZAGA, J
    BOTAS, J
    FERNANDEZAVILES, F
    SORIANO, J
    ESTEBAN, E
    [J]. CIRCULATION, 1992, 85 (03) : 1160 - 1174
  • [7] Initial reperfusion with 2,3 butanedione monoxime is better than hyperkalemic reperfusion after cardioplegic arrest in isolated guinea pig hearts
    Habazettl, H
    Palmisano, BW
    Bosnjak, ZJ
    Stowe, DF
    [J]. EUROPEAN JOURNAL OF CARDIO-THORACIC SURGERY, 1996, 10 (10) : 897 - 904
  • [8] ABRUPT REOXYGENATION OF ANOXIC POTASSIUM-ARRESTED PERFUSED RAT-HEART - STUDY OF MYOCARDIAL ENZYME RELEASE
    HEARSE, DJ
    HUMPHREY, SM
    CHAIN, EB
    [J]. JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1973, 5 (04) : 395 - 407
  • [9] The role of Na+-H+ exchange occurring during hypoxia in the genesis of reoxygenation-induced myocardial oedema
    Inserte, J
    GarciaDorado, D
    RuizMeana, M
    Solares, J
    Soler, J
    [J]. JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1997, 29 (04) : 1167 - 1175
  • [10] Simulated ischemia increases the susceptibility of rat cardiomyocytes to hypercontracture
    Ladilov, YV
    Siegmund, B
    Balser, C
    Piper, HM
    [J]. CIRCULATION RESEARCH, 1997, 80 (01) : 69 - 75