Document Detail

Brief femoral artery ischaemia provides protection against myocardial ischaemia-reperfusion injury in rats: the possible mechanisms.
MedLine Citation:
PMID:  18356557     Owner:  NLM     Status:  MEDLINE    
The present study was conducted to examine the role of nitric oxide (NO), mitochondrial ATP-sensitive K(+) channels (mito K(+)(ATP) channels) and reactive oxygen species (ROS) and their interdependence in brief femoral artery ischaemia-induced myocardial preconditioning. To assess myocardial injury, myocardial infarction was induced by occlusion followed by reperfusion of the left anterior descending (LAD) coronary artery in anaesthetized rats and was assessed by triphenyl tetrazolium chloride (TTC) staining. Left ventricular function was assessed by left ventricular end-diastolic pressure (LVEDP) and the maximal rate of rise of left ventricular pressure [LV(dP/dt)(max)]. Serum creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH) were determined by colorimetric kits. Remote preconditioning (RPC) was induced by 15 min occlusion of femoral arteries followed by 10 min of reperfusion just before LAD coronary artery occlusion. Brief femoral artery ischaemia led to a 61% reduction in myocardial infarct size, 57% reduction in elevated serum LDH and 72% reduction in elevated CK-MB activities, and a significant improvement in LVEDP and LV(dP/dt)(max) compared with control animals. Pretreatment with 5-hydroxydecanoate (5-HD) or l-NAME or N-acetylcystein (NAC) blocked this protective effect of femoral artery ischaemia. Moreover, infusion of l-arginine or diazoxide before coronary artery occlusion markedly reduced the myocardial infarction and improved the left ventricular function. This effect of l-arginine was found to be abolished by the blockade of mito K(+)(ATP) channels with 5-HD and, similarly, the effect of diazoxide was blocked in the presence of a ROS scavenger, NAC. The results suggest that brief femoral artery ischaemia-induced RPC is mediated by a combination of increased NO synthesis, opening of mito K(+)(ATP) channels and increased ROS production. Moreover, it appears that NO is working upstream and acts via activation of mito K(+)(ATP) channels, which subsequently increases the production of ROS.
Mohd Shahid; Mohammad Tauseef; K K Sharma; M Fahim
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-03-20
Journal Detail:
Title:  Experimental physiology     Volume:  93     ISSN:  0958-0670     ISO Abbreviation:  Exp. Physiol.     Publication Date:  2008 Aug 
Date Detail:
Created Date:  2008-07-21     Completed Date:  2008-09-25     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9002940     Medline TA:  Exp Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  954-68     Citation Subset:  IM    
Department of Physiology, Vallabhbhai Patel Chest Institute, University of Delhi, PO Box 2101, Delhi 110007, India.
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MeSH Terms
Arginine / pharmacology
Blood Pressure / physiology
Creatine Kinase, MB Form / blood
Diazoxide / pharmacology
Disease Models, Animal
Femoral Artery / physiopathology*
Heart Rate / physiology
Hindlimb / blood supply
Ischemia / metabolism,  physiopathology*
Ischemic Preconditioning, Myocardial
KATP Channels / metabolism*
L-Lactate Dehydrogenase / blood
Myocardial Infarction / pathology
Myocardial Reperfusion Injury / metabolism,  prevention & control*
Nitric Oxide / metabolism*
Rats, Wistar
Reactive Oxygen Species / metabolism*
Vasodilator Agents
Reg. No./Substance:
0/KATP Channels; 0/Reactive Oxygen Species; 0/Vasodilator Agents; 10102-43-9/Nitric Oxide; 364-98-7/Diazoxide; 74-79-3/Arginine; EC Dehydrogenase; EC Kinase, MB Form

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

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