Document Detail

Responses of chronically hypoxic rat hearts to ischemia: KATP channel blockade does not abolish increased RV tolerance to ischemia.
MedLine Citation:
PMID:  14551060     Owner:  NLM     Status:  MEDLINE    
Chronic hypoxia may precondition the myocardium and protect from ischemia-reperfusion damage. We therefore examined the recovery of left and right ventricular function after ischemia and reperfusion (15 min each) in isolated blood-perfused working hearts from normoxic (Norm) and hypoxic (Hypo; 14 days, 10.5% O(2)) adult rats. In addition, the mRNA expression of hypoxia-inducible factor (HIF)-1alpha and the protein expression of endothelial nitric oxide synthase (eNOS) were measured. Postischemic left ventricular function recovered to 66 +/- 6% and 67 +/- 5% of baseline in Norm and Hypo, respectively. In contrast, postischemic right ventricular function was 93 +/- 2% of baseline in Hypo vs. 67 +/- 3% in Norm (P < 0.05). Improved postischemic right ventricular function in Hypo (93 +/- 2% and 96 +/- 2% of baseline) was observed with 95% O(2) or 21% O(2) in the perfusate, and it was not attenuated by glibenclamide (5 and 10 micromol/l) (86 +/- 4% and 106 +/- 6% recovery). HIF-1alpha mRNA and eNOS protein expression were increased in both left and right hypoxic ventricles. In conclusion, postischemic right, but not left, ventricular function was improved by preceding chronic hypoxia. ATP-sensitive K(+) channels are not responsible for the increased right ventricular tolerance to ischemia after chronic hypoxia in adult rat hearts.
Joerg Forkel; Xiaochao Chen; Susanne Wandinger; Florian Keser; Alexey Duschin; Uwe Schwanke; Stilla Frede; Parwis Massoudy; Rainer Schulz; Heinz Jakob; Gerd Heusch
Publication Detail:
Type:  In Vitro; Journal Article     Date:  2003-10-09
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  286     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2004 Feb 
Date Detail:
Created Date:  2004-01-12     Completed Date:  2004-03-09     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H545-51     Citation Subset:  IM    
Division of Cardiothoracic Surgery, University of Essen, Germany.
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MeSH Terms
ATP-Binding Cassette Transporters
Anoxia / physiopathology*
Body Weight
Carbon Dioxide / blood
Coronary Circulation / physiology
Disease Models, Animal
Heart / physiology,  physiopathology
Hemodynamics / physiology
Hypoxia-Inducible Factor 1, alpha Subunit
Myocardial Ischemia / physiopathology*
Organ Size
Oxygen / blood
Potassium Channel Blockers / pharmacology*
Potassium Channels / drug effects,  physiology*
Potassium Channels, Inwardly Rectifying
RNA, Messenger / genetics
Rats, Wistar
Transcription Factors / genetics
Reg. No./Substance:
0/ATP-Binding Cassette Transporters; 0/Hypoxia-Inducible Factor 1, alpha Subunit; 0/Potassium Channel Blockers; 0/Potassium Channels; 0/Potassium Channels, Inwardly Rectifying; 0/RNA, Messenger; 0/Transcription Factors; 0/uK-ATP-1 potassium channel; 124-38-9/Carbon Dioxide; 7782-44-7/Oxygen

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

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