Document Detail


K(ATP) channel activation reduces the severity of postresuscitation myocardial dysfunction.
MedLine Citation:
PMID:  11009447     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Postresuscitation myocardial dysfunction has been recognized as a leading cause of the high postresuscitation mortality rate. We investigated the effects of ischemic preconditioning and activation of ATP-sensitive K(+) (K(ATP)) channels on postresuscitation myocardial function. Ventricular fibrillation (VF) was induced in 25 Sprague-Dawley rats. Cardiopulmonary resuscitation (CPR), including mechanical ventilation and precordial compression, was initiated after 4 min of untreated VF. Defibrillation was attempted after 6 min of CPR. The animals were randomized to five groups treated with 1) ischemic preconditioning, 2) K(ATP) channel opener, 3) ischemic preconditioning with K(ATP) channel blocker administered 1 min after VF, 4) K(ATP) channel blocker administered 45 min before induction of ischemic preconditioning, and 5) placebo. Postresuscitation myocardial function, as measured by the rate of left ventricular pressure increase at 40 mmHg, the rate of left ventricular decline, cardiac index, and duration of survival, was significantly improved in both preconditioned and K(ATP) channel opener-treated animals. K(ATP) channel blocker administered 45 min before induction of ischemic preconditioning completely abolished the myocardial protective effects of preconditioning. We conclude that ischemic preconditioning significantly improved post-CPR myocardial function and survival. These results also provide evidence that the myocardial protective effects of ischemic preconditioning are mediated by K(ATP) channel activation.
Authors:
W Tang; M H Weil; S Sun; A Pernat; E Mason
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  279     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2000 Oct 
Date Detail:
Created Date:  2000-10-23     Completed Date:  2000-11-07     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  H1609-15     Citation Subset:  IM    
Affiliation:
Institute of Critical Care Medicine, Palm Springs 92262, California, USA.
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MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphate / physiology*
Animals
Antihypertensive Agents / therapeutic use
Blood Pressure / drug effects
Cardiac Complexes, Premature / epidemiology
Coronary Circulation
Cromakalim / therapeutic use
Glyburide / therapeutic use
Heart / physiopathology*
Incidence
Ischemic Preconditioning, Myocardial
Perfusion
Potassium Channels / physiology*
Rats
Rats, Sprague-Dawley
Resuscitation*
Survival Analysis
Grant Support
ID/Acronym/Agency:
HL-54322/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Antihypertensive Agents; 0/Potassium Channels; 10238-21-8/Glyburide; 56-65-5/Adenosine Triphosphate; 94470-67-4/Cromakalim

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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