Document Detail


Myocardial protection with intermittent cross-clamp fibrillation: does preconditioning play a role?
MedLine Citation:
PMID:  16242951     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: Previously, we showed intermittent cross-clamp fibrillation afforded equivalent protection to cardioplegia. This study examined whether protection induced by intermittent cross-clamp fibrillation involves an ischemic preconditioning mechanism. METHODS: Isolated Langendorff-perfused rat hearts were subjected to three different studies to determine: Study 1, whether a single intermittent cross-clamp fibrillation episode (10 min) and reperfusion (10 min) before prolonged ischemia acts as a preconditioning trigger for protection; Study 2, whether cardioprotection induced by intermittent cross-clamp fibrillation alone (no prolonged ischemia) involves a preconditioning mechanism; Study 3, whether intermittent cross-clamp fibrillation cardioprotection can be prevented by targeting putative components of the preconditioning mechanism (protein kinase C or the mitochondrial ATP-sensitive potassium (K(ATP)) channel). Hearts were reperfused (60 min) and recovery of function (left ventricular developed pressure measured using an intraventricular balloon) and myocardial injury (creatine kinase leakage) were measured. RESULTS: In Study 1, recovery of function in the single intermittent cross-clamp fibrillation hearts was 61+/-3% (mean+/-SEM) (p<0.05) compared to 41+/-2% in control group; glibenclamide (a non-specific ATP-sensitive potassium (K(ATP))-channel blocker) prevented this preconditioning protection (37+/-4%). In Study 2, recovery of function in intermittent cross-clamp fibrillation hearts (62+/-3%) was significantly (p<0.05) higher than intermittent cross-clamp fibrillation hearts treated with glibenclamide (33+/-2%) and ischemia hearts (30+/-5%). In Study 3, protection by intermittent cross-clamp fibrillation (60+/-3%; p<0.05) was attenuated by protein kinase C inhibition (chelerythrine, 34+/-3%) and mitochondrial K(ATP)-channel blockade (5-hydroxydecanoate, 27+/-4%) to levels not significantly different from that of ischemia hearts (25+/-4%). CONCLUSIONS: The cardioprotective efficacy of intermittent cross-clamp fibrillation was attenuated by protein kinase C inhibition or K(ATP)-channel blockade. Involvement of these putative preconditioning cascade components in association with cardioprotection induced by intermittent cross-clamp fibrillation, suggests a role for the ischemic preconditioning mechanism.
Authors:
Masahiro Fujii; David J Chambers
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2005-10-20
Journal Detail:
Title:  European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery     Volume:  28     ISSN:  1010-7940     ISO Abbreviation:  Eur J Cardiothorac Surg     Publication Date:  2005 Dec 
Date Detail:
Created Date:  2005-12-05     Completed Date:  2006-03-22     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  8804069     Medline TA:  Eur J Cardiothorac Surg     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  821-31     Citation Subset:  IM    
Affiliation:
Cardiac Surgical Research/Cardiothoracic Surgery, The Rayne Institute, Guy's and St Thomas' NHS Foundation Trust, St Thomas' Hospital, London SE1 7EH, UK.
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MeSH Terms
Descriptor/Qualifier:
Animals
Constriction
Coronary Artery Bypass
Creatine Kinase / metabolism
Glyburide / pharmacology
Ischemic Preconditioning, Myocardial / methods*
Male
Myocardial Reperfusion Injury / prevention & control*
Myocardium / metabolism
Organ Culture Techniques
Potassium Channel Blockers / pharmacology
Potassium Channels / physiology
Protein Kinase C / antagonists & inhibitors,  physiology
Rats
Rats, Wistar
Recovery of Function
Ventricular Fibrillation
Ventricular Function, Left
Chemical
Reg. No./Substance:
0/Potassium Channel Blockers; 0/Potassium Channels; 0/mitochondrial K(ATP) channel; 10238-21-8/Glyburide; EC 2.7.11.13/Protein Kinase C; EC 2.7.3.2/Creatine Kinase
Comments/Corrections
Comment In:
Eur J Cardiothorac Surg. 2005 Dec;28(6):831-2   [PMID:  16275003 ]
Eur J Cardiothorac Surg. 2006 May;29(5):860; author reply 861   [PMID:  16520049 ]

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