期刊
CARDIOVASCULAR RESEARCH
卷 72, 期 2, 页码 220-230出版社
OXFORD UNIV PRESS
DOI: 10.1016/j.cardiores.2006.07.011
关键词
K-ATP channel; sepsis; septic shock; vascular hyporeactivity; multi-organ failure; mitochondria; insulin
资金
- British Heart Foundation [FS/02/068/14402, FS/02/068/14402] Funding Source: Medline
- Medical Research Council [G117/440, G117/440(77598)] Funding Source: Medline
- Wellcome Trust Funding Source: Medline
- Medical Research Council [G117/440] Funding Source: researchfish
- MRC [G117/440] Funding Source: UKRI
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.
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