Document Detail

Taurine protects the heart from neutrophil-induced reperfusion injury.
MedLine Citation:
PMID:  7590395     Owner:  NLM     Status:  MEDLINE    
Deficiency of the amino acid taurine is implicated in various pathologic states of the heart. Besides other effects, taurine has been proposed to be an antioxidant. However, its benefit under conditions associated with the generation of reactive oxygen species in the heart has not been clearly demonstrated. To assess the potential of taurine to influence neutrophil-dependent reperfusion injury, a model was developed based on the isolated working guinea pig heart. After an initial work phase, hearts were subjected to 15 min of global ischemia. Reperfusion, in a nonworking mode, was carried out in the absence or presence of homologous neutrophils (PMN) and/or taurine. After 15 min, work was resumed and percentage recovery of function was determined another 20 min later. During the reperfusion phase, coronary venous effluent was collected to quantify release of lactate and glutathione, markers of ischemic challenge and redox-stress, respectively. Furthermore, direct effects of taurine on radical formation were investigated in a chemiluminescence assay. Control hearts without application of PMN or taurine had a postischemic recovery of external heart work (EHW) of 76%, in the presence of taurine (15 mM) recovery was 72%. The application of PMN for merely the first minute of reperfusion led to a significant decrease in recovery to 30%, PMN having no effect without a foregoing ischemia. When taurine was additionally applied during reperfusion, EHW recovered to 60%. Release of lactate and of oxidized glutathione (GSSG) did not differ between the groups. In contrast, effluent concentrations of reduced glutathione (GSH) were considerably elevated by the presence of PMN in the sample and remained high even after PMN-washout. Taurine tended to attenuate this PMN effect. At the 5th and 10th min of reperfusion, GSH release of individual hearts correlated inversely with postischemic recovery of EHW. Surprisingly, taurine, by itself, did not significantly alter glutathione release. However, taurine (15 mM) markedly reduced luminol-dependent chemiluminescence elicited by activated guinea pig PMN as well as by chemically generated hypochlorous acid and hydroxyl radicals, but not superoxide radicals. Our results demonstrate that taurine protects the heart from PMN-induced reperfusion injury and oxidative stress. Because respiratory burst activity of PMN was also significantly reduced in the presence of taurine, the beneficial effect appears to be mediated by antioxidative properties of taurine.
P Raschke; P Massoudy; B F Becker
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Free radical biology & medicine     Volume:  19     ISSN:  0891-5849     ISO Abbreviation:  Free Radic. Biol. Med.     Publication Date:  1995 Oct 
Date Detail:
Created Date:  1995-12-08     Completed Date:  1995-12-08     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8709159     Medline TA:  Free Radic Biol Med     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  461-71     Citation Subset:  IM    
Physiologisches Institut, Universität München, Germany.
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MeSH Terms
Antioxidants / therapeutic use*
Chemiluminescent Measurements
Coronary Vessels
Glutathione / blood
Guinea Pigs
Heart / drug effects,  physiology
Lactates / blood
Lactic Acid
Luminol / pharmacology
Myocardial Reperfusion Injury / prevention & control*
Neutrophils / drug effects,  physiology*
Respiratory Burst / drug effects
Taurine / pharmacology,  therapeutic use*
Reg. No./Substance:
0/Antioxidants; 0/Lactates; 107-35-7/Taurine; 50-21-5/Lactic Acid; 521-31-3/Luminol; 70-18-8/Glutathione

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

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