Myocardial protection by nitrite

被引:60
作者
Calvert, John W. [1 ]
Lefer, David J. [1 ]
机构
[1] Emory Univ, Dept Surg, Div Cardiothorac Surg, Sch Med,Carlyle Fraser Heart Ctr,Crawford Long Ho, Atlanta, GA 30308 USA
基金
美国国家卫生研究院;
关键词
Nitric oxide; Nitrite; Cardioprotection; Myocardial ischaemia; Acute myocardial infarction; VIVO ISCHEMIA-REPERFUSION; OXIDE SYNTHASE ACTIVITY; ENDOTHELIAL DYSFUNCTION; IN-VIVO; ISCHEMIA/REPERFUSION INJURY; PROTEIN-KINASE; SODIUM-NITRITE; INHALED NO; SIGNALING MOLECULE; RELAXING FACTOR;
D O I
10.1093/cvr/cvp079
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Nitrite has long been considered to be an inert oxidative metabolite of nitric oxide (NO). Recent work, however, has demonstrated that nitrite represents an important tissue storage form of NO that can be reduced to NO during ischaemic or hypoxic events. This exciting series of discoveries has created an entirely new field of research that involves the investigation of the molecular, biochemical, and physiological activities of nitrite under a variety of physiological and pathophysiological states. This has also led to a re-evaluation of the role that nitrite plays in health and disease. As a result there has been an interest in the use of nitrite as a therapeutic strategy for the treatment of acute myocardial infarction. Nitrite therapy has now been studied in several animal models and has proven to be an effective means to reduce myocardial ischaemia-reperfusion injury. This review article will provide a brief summary of the key findings that have led to the re-evaluation of nitrite and highlight the evidence supporting the cardioprotective actions of nitrite and also highlight the potential clinical application of nitrite therapy to cardiovascular diseases.
引用
收藏
页码:195 / 203
页数:9
相关论文
共 113 条
[32]   Inhaled nitric oxide decreases infarction size and improves left ventricular function in a murine model of myocardial ischemia-reperfusion injury [J].
Hataishi, Ryuji ;
Rodrigues, Ana Clara ;
Neilan, Tomas G. ;
Morgan, John G. ;
Buys, Emmanuel ;
Shiva, Sruti ;
Tambouret, Rosemary ;
Jassal, Davinder S. ;
Raher, Michael J. ;
Furutani, Elissa ;
Ichinose, Fumito ;
Gladwin, Mark T. ;
Rosenzweig, Anthony ;
Zapol, Warren M. ;
Picard, Michael H. ;
Bloch, Kenneth D. ;
Scherrer-Crosbie, Marielle .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2006, 291 (01) :H379-H384
[33]   Plasma nitroso compounds are decreased in patients with endothelial dysfunction [J].
Heiss, C ;
Lauer, T ;
Dejam, A ;
Kleinbongard, P ;
Hamada, S ;
Rassaf, T ;
Matern, S ;
Feelisch, M ;
Kelm, M .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2006, 47 (03) :573-579
[34]   Endothelial dysfunction, oxidative stress, and risk of cardiovascular events in patients with coronary artery disease [J].
Heitzer, T ;
Schlinzig, T ;
Krohn, K ;
Meinertz, T ;
Münzel, T .
CIRCULATION, 2001, 104 (22) :2673-2678
[35]  
Hink U, 2001, CIRC RES, V88, pE14
[36]  
HOGG N, 2007, FREE RADIC BIOL MED
[37]  
Hu H, 1997, CIRC RES, V81, P742
[38]   Nitric oxide: A unique endogenous signaling molecule in vascular biology [J].
Ignarro, LJ .
BIOSCIENCE REPORTS, 1999, 19 (02) :51-71
[39]   ENDOTHELIUM-DERIVED RELAXING FACTOR PRODUCED AND RELEASED FROM ARTERY AND VEIN IS NITRIC-OXIDE [J].
IGNARRO, LJ ;
BUGA, GM ;
WOOD, KS ;
BYRNS, RE ;
CHAUDHURI, G .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1987, 84 (24) :9265-9269
[40]  
JOHNSON G, 1990, J PHARMACOL EXP THER, V252, P35