Role of KATP channels in sepsis

被引:76
作者
Buckley, James F. [1 ]
Singer, Mervyn [1 ]
Clapp, Lucie H. [1 ]
机构
[1] UCL, BHF Labs, Dept Med, London WC1E 6JF, England
基金
英国医学研究理事会; 英国惠康基金;
关键词
K-ATP channel; sepsis; septic shock; vascular hyporeactivity; multi-organ failure; mitochondria; insulin;
D O I
10.1016/j.cardiores.2006.07.011
中图分类号
R5 [内科学];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
Sepsis is an infection-induced inflammatory syndrome responsible for similar to 10% of all deaths worldwide. While pathophysiological mechanisms remain to be fully unravelled, new insights and discoveries are yielding significant improvements in outcome, particularly in the high mortality conditions of shock and multi-organ failure. One potential target is the ATP-sensitive potassium (K-ATP) channel, an ion channel critical to the cardiovascular stress response. Excessive activation of the vascular channel is now recognised as a major cause of hypotension and vascular hyporesponsiveness to catecholamines in septic shock. Some researchers advocate therapeutic blockade of these channels; however, outside the vasculature, channel opening may actually represent a protective mechanism against cellular damage. In this review we critically examine the role of the K-ATP channel in sepsis. (c) 2006 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:220 / 230
页数:11
相关论文
共 109 条
[1]
RETRACTED: The large-conductance Ca2+-activated K+ channel is essential for innate immunity (Retracted article. See vol. 468, 2010) [J].
Ahluwalia, J ;
Tinker, A ;
Clapp, LH ;
Duchen, MR ;
Abramov, AY ;
Pope, S ;
Nobles, M ;
Segal, AW .
NATURE, 2004, 427 (6977) :853-858
[2]
Myocardial ischemia induces differential regulation of KATP channel gene expression in rat hearts [J].
Akao, M ;
Otani, H ;
Horie, M ;
Takano, M ;
Kuniyasu, A ;
Nakayama, H ;
Kouchi, I ;
Sasayama, S ;
Murakami, T .
JOURNAL OF CLINICAL INVESTIGATION, 1997, 100 (12) :3053-3059
[3]
Mitochondrial ATP-sensitive potassium channels inhibit apoptosis induced by oxidative stress in cardiac cells [J].
Akao, M ;
Ohler, A ;
O'Rourke, B ;
Marbán, E .
CIRCULATION RESEARCH, 2001, 88 (12) :1267-1275
[4]
Primer - Cellular regulation of actin network assembly [J].
Amann, KJ ;
Pollard, TD .
CURRENT BIOLOGY, 2000, 10 (20) :R728-R730
[5]
Septic shock [J].
Annane, D ;
Bellissant, E ;
Cavaillon, JM .
LANCET, 2005, 365 (9453) :63-78
[6]
Glucocorticoids in the treatment of severe sepsis and septic shock [J].
Annane, D .
CURRENT OPINION IN CRITICAL CARE, 2005, 11 (05) :449-453
[7]
Compartmentalised inducible nitric-oxide synthase activity in septic shock [J].
Annane, D ;
Sanquer, S ;
Sébille, V ;
Faye, A ;
Djuranovic, D ;
Raphaël, JC ;
Gajdos, P ;
Bellissant, E .
LANCET, 2000, 355 (9210) :1143-1148
[8]
Mitochondrial KATP channels in cell survival and death [J].
Ardehali, H ;
O'Rourke, B .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2005, 39 (01) :7-16
[9]
CHANGES IN PLASMA-CONCENTRATIONS OF VASOACTIVE NEUROPEPTIDES IN PATIENTS WITH SEPSIS AND SEPTIC SHOCK [J].
ARNALICH, F ;
SANCHEZ, JF ;
MARTINEZ, M ;
JIMENEZ, M ;
LOPEZ, J ;
VAZQUEZ, JJ ;
HERNANZ, A .
LIFE SCIENCES, 1994, 56 (02) :75-81
[10]
Nitric oxide-dependent generation of reactive species in sickle cell disease - Actin tyrosine nitration induces defective cytoskeletal polymerization [J].
Aslan, M ;
Ryan, TM ;
Townes, TM ;
Coward, L ;
Kirk, MC ;
Barnes, S ;
Alexander, CB ;
Rosenfeld, SS ;
Freeman, BA .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (06) :4194-4204