Role of KATP channels in sepsis
Sepsis is an infection-induced inflammatory syndrome responsible for approximately 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 conditi...
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Veröffentlicht in: | Cardiovascular research 2006-11, Vol.72 (2), p.220-230 |
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description | Sepsis is an infection-induced inflammatory syndrome responsible for approximately 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. |
doi_str_mv | 10.1016/j.cardiores.2006.07.011 |
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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. 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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.</description><subject>Adenosine Triphosphate - metabolism</subject><subject>Bacterial diseases</subject><subject>Bacterial sepsis</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Human bacterial diseases</subject><subject>Humans</subject><subject>Infectious diseases</subject><subject>Ischemic Preconditioning</subject><subject>Medical sciences</subject><subject>Multiple Organ Failure - metabolism</subject><subject>Potassium Channels - metabolism</subject><subject>Sepsis - metabolism</subject><subject>Vasodilation</subject><issn>0008-6363</issn><issn>1755-3245</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkE1Lw0AQhhdRbK3-BZuL3hJnM_uRHEupH1hQpJ6XzXaDKWlSd-zBf--WBnsaXnjemeFhbMoh48DVwyZzNqybPnjKcgCVgc6A8zM25lrKFHMhz9kYAIpUocIRuyLaxCilFpdsxFWpMKYxm370rU_6Onmdrd4T92W7zreUNF1CfkcNXbOL2rbkb4Y5YZ-Pi9X8OV2-Pb3MZ8vUIUie5mCLWmA8LlylvNSKqxwdVrnmUqhSaJ-jkNIjoNNWrwtdSCirutaFRalwwu6Pe3eh_957-jHbhpxvW9v5fk9GFWX8WfII6iPoQk8UfG12odna8Gs4mIMbszH_bszBjQFtopvYvB1O7KutX596g4wI3A2AJWfbOtjONXTiipyj1gr_AJ42a-I</recordid><startdate>20061101</startdate><enddate>20061101</enddate><creator>BUCKLEY, James F</creator><creator>SINGER, Mervyn</creator><creator>CLAPP, Lucie H</creator><general>Oxford University Press</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20061101</creationdate><title>Role of KATP channels in sepsis</title><author>BUCKLEY, James F ; SINGER, Mervyn ; CLAPP, Lucie H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3051-20a8f431754cb6e5761623c3b271546947e23455e303c7a7d878509bff78a3563</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adenosine Triphosphate - metabolism</topic><topic>Bacterial diseases</topic><topic>Bacterial sepsis</topic><topic>Biological and medical sciences</topic><topic>Cardiology. 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source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Oxford University Press Journals All Titles (1996-Current); Alma/SFX Local Collection |
subjects | Adenosine Triphosphate - metabolism Bacterial diseases Bacterial sepsis Biological and medical sciences Cardiology. Vascular system Human bacterial diseases Humans Infectious diseases Ischemic Preconditioning Medical sciences Multiple Organ Failure - metabolism Potassium Channels - metabolism Sepsis - metabolism Vasodilation |
title | Role of KATP channels in sepsis |
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