Document Detail


Loss of glycogen during preconditioning is not a prerequisite for protection of the rabbit heart.
MedLine Citation:
PMID:  8922255     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Depletion of glycogen has been proposed as the mechanism of protection from ischemic preconditioning. The hypothesis was tested by seeing whether pharmacological manipulation of preconditioning causes parallel changes in cardiac glycogen content. Five groups of isolated rabbit hearts were studied. Group 1 experienced 30 min of ischemia only. Group 2 (PC) was preconditioned with 5 min of global ischemia followed by 10 min of reperfusion. Group 3 was preconditioned with 5 min exposure to 400 nM bradykinin followed by a 10 min washout period. Group 4 experienced exposure to 10 microM adenosine followed by a 10 min washout period, and the fifth group was also preconditioned with 5 min ischemia and 10 min reperfusion but 100 microM 8-(p-sulfophenyl)theophylline (SPT), which blocks adenosine receptors, was included in the buffer to block preconditioning's protection. Transmural biopsies were taken before treatment, just prior to the 30 min period of global ischemia, and after 30 min of global ischemia. Glycogen in the samples was digested with amyloglucosidase and the resulting glucose was assayed. Baseline glycogen averaged 17.3 +/- 0.6 mumol glucose/g wet weight. After preconditioning glycogen decreased to 13.3 +/- 1.3 mumol glucose/g wet weight (p < 0.005 vs. baseline). Glycogen was similarly depleted after pharmacological preconditioning with adenosine (14.0 +/- 1.0 mumol glucose/g wet weight, p < 0.05 vs. baseline) suggesting a correlation. However, when preconditioning was performed in the presence of SPT, which blocks protection, glycogen was also depleted by the same amount (13.3 +/- 0.7 mumol glucose/g wet weight, p = ns vs. PC). Bradykinin, which also mimics preconditioning, caused no depletion of glycogen (16.3 +/- 0.8 mumol glucose/g wet weight, p = ns vs. baseline). Because preconditioning with bradykinin did not deplete glycogen and because glycogen continued to be low when protection from preconditioning was blocked with SPT, we conclude that loss of glycogen per se does not cause the protection of preconditioning.
Authors:
C Weinbrenner; P Wang; J M Downey
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Basic research in cardiology     Volume:  91     ISSN:  0300-8428     ISO Abbreviation:  Basic Res. Cardiol.     Publication Date:    1996 Sep-Oct
Date Detail:
Created Date:  1997-02-27     Completed Date:  1997-02-27     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0360342     Medline TA:  Basic Res Cardiol     Country:  GERMANY    
Other Details:
Languages:  eng     Pagination:  374-81     Citation Subset:  IM    
Affiliation:
Department of Physiology, University of South Alabama, College of Medicine, Mobile 36688, USA.
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MeSH Terms
Descriptor/Qualifier:
Adenosine / pharmacology
Animals
Biopsy
Blood Flow Velocity / drug effects
Bradykinin / pharmacology
Coronary Vessels / drug effects
Female
Glycogen / metabolism*
Ischemic Preconditioning, Myocardial / adverse effects*
Male
Myocardial Ischemia / metabolism*,  pathology,  physiopathology
Rabbits
Spectrophotometry
Theophylline / pharmacology
Vasodilator Agents / pharmacology
Grant Support
ID/Acronym/Agency:
HL 20648/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Vasodilator Agents; 58-55-9/Theophylline; 58-61-7/Adenosine; 58-82-2/Bradykinin; 9005-79-2/Glycogen

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


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