Document Detail

Repeated physiologic stresses provide persistent cardioprotection against ischemia-reperfusion injury in rats.
MedLine Citation:
PMID:  12204517     Owner:  NLM     Status:  MEDLINE    
OBJECTIVES: We investigated the time course of myocardial tolerance to ischemia-reperfusion injury after repeated physiologic or pharmacologic stresses. BACKGROUND: Sublethal stress provides cardiac tolerance to ischemia-reperfusion injury and increases the activity of manganese superoxide dismutase (Mn-SOD) in the myocardium in a biphasic manner. However, few studies have investigated the time course of the cardioprotective effects after repeated stresses. METHODS: One or two episodes of the same physiologic or pharmacologic stress (exercise, whole-body hyperthermia, or tumor necrosis factor-alpha treatment), or a combination of two different types of stress, were induced after a 48-h interval. The rats were then subjected to 20 min of left coronary artery occlusion, followed by 48 h of reperfusion. The interval between the last stimulus and the induced ischemia was between 0.5 h and 168 h. The incidence of ventricular fibrillation during ischemia and the size of the myocardial infarct after reperfusion were then examined. RESULTS: When two episodes of physiologic or pharmacologic stress were induced, the beneficial effects against ischemia-reperfusion injury were observed in a monophasic manner. These effects persisted for a period of 0.5 to 60 h. One episode of sublethal stress provoked the same beneficial effects, but in a biphasic manner. The increase in Mn-SOD activity in the cardiac tissue resembled the time course for cardioprotection against ischemia-reperfusion injury. CONCLUSIONS: Two episodes of physiologic or pharmacologic stress can provide persistent cardioprotective effects against ischemia-reperfusion injury.
Shiro Hoshida; Nobushige Yamashita; Kinya Otsu; Masatsugu Hori
Related Documents :
19696117 - Plasma mir-208 as a biomarker of myocardial injury.
3838707 - Failure of the xanthine oxidase inhibitor allopurinol to limit infarct size after ische...
22292457 - Type of desmin expression in cardiomyocytes -a good marker of heart failure development...
25128167 - Regulatory t cells are recruited in the infarcted mouse myocardium and may modulate fib...
19696117 - Plasma mir-208 as a biomarker of myocardial injury.
11300457 - Noninvasive detection and evaluation of atherosclerotic coronary plaques with multislic...
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of the American College of Cardiology     Volume:  40     ISSN:  0735-1097     ISO Abbreviation:  J. Am. Coll. Cardiol.     Publication Date:  2002 Aug 
Date Detail:
Created Date:  2002-09-02     Completed Date:  2002-09-17     Revised Date:  2004-11-17    
Medline Journal Info:
Nlm Unique ID:  8301365     Medline TA:  J Am Coll Cardiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  826-31     Citation Subset:  AIM; IM    
Division of Cardiology, Osaka Rosai Hospital, Sakai, Japan.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Hyperthermia, Induced*
Myocardial Infarction / drug therapy*,  physiopathology
Myocardial Reperfusion Injury / physiopathology,  prevention & control*
Physical Conditioning, Animal*
Rats, Wistar
Tumor Necrosis Factor-alpha / pharmacology,  therapeutic use*
Reg. No./Substance:
0/Tumor Necrosis Factor-alpha

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

Previous Document:  Production of 8-epi prostaglandin F(2alpha) in human platelets during administration of organic nitr...
Next Document:  Resistance in the land of molecular cancer therapeutics.