Negative inotropic mediators released from the heart after myocardial ischaemia-reperfusion

被引:51
作者
Stangl, V
Baumann, G
Stangl, K
Felix, SB
机构
[1] Humboldt Univ, Med Klin, Charite, D-10098 Berlin, Germany
[2] Ernst Moritz Arndt Univ Greifswald, Klin Innere Med B, Greifswald, Germany
关键词
cytokines; free radicals; ischemia; macrophages; myocytes; nitric oxide; reperfusion;
D O I
10.1016/S0008-6363(01)00420-5
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The heart responds to ischaemic stimuli with release of negative inotropic mediators such as cytokines, platelet-activating factor, oxygen free radicals, arachidonic acids, nitric oxide, adenosine, and still unidentified "cardiodepressant factors" that modulate myocardial performance via autocrine and paracrine coupling. This review summarises experimental and clinical data on the role of negative inotropic mediators that are released from cardiac cells (including cardiomyocytes, endothelial cells, and resident mast cells) after myocardial ischaemia-reperfusion. (C) 2002 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:12 / 30
页数:19
相关论文
共 265 条
  • [21] DEMONSTRATION OF FREE-RADICAL GENERATION IN STUNNED MYOCARDIUM OF INTACT DOGS WITH THE USE OF THE SPIN TRAP ALPHA-PHENYL N-TERT-BUTYL NITRONE
    BOLLI, R
    PATEL, BS
    JEROUDI, MO
    LAI, EK
    MCCAY, PB
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1988, 82 (02) : 476 - 485
  • [22] MARKED REDUCTION OF FREE-RADICAL GENERATION AND CONTRACTILE DYSFUNCTION BY ANTIOXIDANT THERAPY BEGUN AT THE TIME OF REPERFUSION - EVIDENCE THAT MYOCARDIAL STUNNING IS A MANIFESTATION OF REPERFUSION INJURY
    BOLLI, R
    JEROUDI, MO
    PATEL, BS
    ARUOMA, OI
    HALLIWELL, B
    LAI, EK
    MCCAY, PB
    [J]. CIRCULATION RESEARCH, 1989, 65 (03) : 607 - 622
  • [23] Molecular and cellular mechanisms of myocardial stunning
    Bolli, R
    Marbán, E
    [J]. PHYSIOLOGICAL REVIEWS, 1999, 79 (02) : 609 - 634
  • [24] DIRECT EVIDENCE THAT OXYGEN-DERIVED FREE-RADICALS CONTRIBUTE TO POSTISCHEMIC MYOCARDIAL DYSFUNCTION IN THE INTACT DOG
    BOLLI, R
    JEROUDI, MO
    PATEL, BS
    DUBOSE, CM
    LAI, EK
    ROBERTS, R
    MCCAY, PB
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1989, 86 (12) : 4695 - 4699
  • [25] Pathophysiologically relevant concentrations of tumor necrosis factor-α promote progressive left ventricular dysfunction and remodeling in rats
    Bozkurt, B
    Kribbs, SB
    Clubb, FJ
    Michael, LH
    Didenko, VV
    Hornsby, PJ
    Seta, Y
    Oral, H
    Spinale, FG
    Mann, DL
    [J]. CIRCULATION, 1998, 97 (14) : 1382 - 1391
  • [26] NITRIC-OXIDE ATTENUATES CARDIAC MYOCYTE CONTRACTION
    BRADY, AJB
    WARREN, JB
    POOLEWILSON, PA
    WILLIAMS, TJ
    HARDING, SE
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY, 1993, 265 (01): : H176 - H182
  • [27] Heterogeneous basal expression of nitric oxide synthase and superoxide dismutase isoforms in mammalian heart - Implications for mechanisms governing indirect and direct nitric oxide-related effects
    Brahmajothi, MV
    Campbell, DL
    [J]. CIRCULATION RESEARCH, 1999, 85 (07) : 575 - 587
  • [28] THE STUNNED MYOCARDIUM - PROLONGED, POST-ISCHEMIC VENTRICULAR DYSFUNCTION
    BRAUNWALD, E
    KLONER, RA
    [J]. CIRCULATION, 1982, 66 (06) : 1146 - 1149
  • [29] EFFECTS OF DAMAGING THE ENDOCARDIAL SURFACE ON THE MECHANICAL PERFORMANCE OF ISOLATED CARDIAC-MUSCLE
    BRUTSAERT, DL
    MEULEMANS, AL
    SIPIDO, KR
    SYS, SU
    [J]. CIRCULATION RESEARCH, 1988, 62 (02) : 358 - 366
  • [30] THE ENDOCARDIAL ENDOTHELIUM
    BRUTSAERT, DL
    ANDRIES, LJ
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY, 1992, 263 (04): : H985 - H1002