Pathogenesis of Myocardial Ischemia-Reperfusion Injury and Rationale for Therapy

被引:598
作者
Turer, Aslan T. [1 ]
Hill, Joseph A. [1 ,2 ]
机构
[1] Univ Texas SW Med Ctr Dallas, Dept Internal Med Cardiol, Dallas, TX 75390 USA
[2] Univ Texas SW Med Ctr Dallas, Dept Mol Biol, Dallas, TX 75390 USA
基金
美国国家卫生研究院;
关键词
MITOCHONDRIAL PERMEABILITY TRANSITION; PERCUTANEOUS CORONARY INTERVENTION; BYPASS GRAFT-SURGERY; NO-REFLOW PHENOMENON; HYDROGEN EXCHANGE INHIBITION; FREE-RADICAL GENERATION; REDUCES INFARCT SIZE; NITRIC-OXIDE; CONTROLLED-TRIAL; CARDIAC-SURGERY;
D O I
10.1016/j.amjcard.2010.03.032
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Since the initial description of the phenomenon by Jennings et al 50 years ago, our understanding of the underlying mechanisms of reperfusion injury has grown significantly. Its pathogenesis reflects the confluence of multiple pathways, including ion channels, reactive oxygen species, inflammation, and endothelial dysfunction. The purposes of this review are to examine the current state of understanding of ischemia-reperfusion injury, as well as to highlight recent interventions aimed at this heretofore elusive target. In conclusion, despite its complexity our ongoing efforts to mitigate this form of injury should not be deterred, because nearly 2 million patients annually undergo either spontaneous (in the form of acute myocardial infarction) or iatrogenic (in the context of cardioplegic arrest) ischemia-reperfusion. (C) 2010 Elsevier Inc. All rights reserved. (Am J Cardiol 2010;106: 360-368)
引用
收藏
页码:360 / 368
页数:9
相关论文
共 136 条
[61]  
LELL W, 1995, ANESTHESIOLOGY, V83, P658
[62]  
Lemasters J J, 1996, EXS, V76, P99
[63]  
LEUNG JM, 1994, ANESTH ANALG, V78, P420
[64]   Cardiopulmonary and systemic effects of methylprednisolone in patients undergoing cardiac surgery [J].
Liakopoulos, Oliver J. ;
Schmitto, Jan D. ;
Kazmaier, Stefan ;
Braeuer, Anselm ;
Quintel, Michael ;
Schoendube, Friedrich A. ;
Doerge, Hilmar .
ANNALS OF THORACIC SURGERY, 2007, 84 (01) :110-119
[65]   Post-conditioning reduces infarct size in an open-chest porcine acute ischemia-reperfusion model [J].
Lie, R. H. ;
Hasenkam, J. M. ;
Nielsen, T. T. ;
Poulsen, R. ;
Sloth, E. .
ACTA ANAESTHESIOLOGICA SCANDINAVICA, 2008, 52 (09) :1188-1193
[66]   PROTECTION AGAINST INFARCTION AFFORDED BY PRECONDITIONING IS MEDIATED BY A1 ADENOSINE RECEPTORS IN RABBIT HEART [J].
LIU, GS ;
THORNTON, J ;
VANWINKLE, DM ;
STANLEY, AWH ;
OLSSON, RA ;
DOWNEY, JM .
CIRCULATION, 1991, 84 (01) :350-356
[67]  
Lloyd-Jones D, 2009, CIRCULATION, V121, pe1
[68]  
Loke KE, 1999, CIRC RES, V84, P840
[69]   DIMINISHED BASAL NITRIC-OXIDE RELEASE AFTER MYOCARDIAL-ISCHEMIA AND REPERFUSION PROMOTES NEUTROPHIL ADHERENCE TO CORONARY ENDOTHELIUM [J].
MA, XL ;
WEYRICH, AS ;
LEFER, DJ ;
LEFER, AM .
CIRCULATION RESEARCH, 1993, 72 (02) :403-412
[70]   Adenosine as an adjunct to thrombolytic therapy for acute myocardial infarction - Results of a multicenter, randomized, placebo-controlled trial: The Acute Myocardial Infarction STudy of ADenosine (AMISTAD) Trial [J].
Mahaffey, KW ;
Puma, JA ;
Barbagelata, NA ;
DiCarli, MF ;
Leesar, MA ;
Browne, KF ;
Eisenberg, PR ;
Bolli, R ;
Casas, AC ;
Molina-Viamonte, V ;
Orlandi, C ;
Blevins, R ;
Gibbons, RJ ;
Califf, RM ;
Granger, CB .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1999, 34 (06) :1711-1720