Document Detail

Antioxidant properties of acetaminophen and cardioprotection.
MedLine Citation:
PMID:  11605988     Owner:  NLM     Status:  MEDLINE    
The acute administration of acetaminophen to isolated, perfused guinea pig hearts appears to have cardioprotective effects against the injury/mechanical dysfunction caused by global, low-flow, myocardial ischemia and reperfusion. In the current study we selected ischemia/reperfusion and administration of sodium pentobarbital as perturbations of the electrical stability of the myocardium. We investigated their ability to induce ventricular arrhythmias and changes in the characteristics of monophasic action potentials in the absence and presence of acetaminophen (0.35 mmol/l). The numbers of ventricular premature beats and ventricular salvos encountered in the presence of pentobarbital were significantly (P < 0.05) reduced by acetaminophen. The combined frequency of these arrhythmias was 0.14+/-0.06/min vs 0.03+/-0.01/min (P < 0.05) in the absence and presence of acetaminophen, respectively. The incidence of ventricular salvos increased steadily in vehicle-treated hearts after administration of pentobarbital. No such trend was seen with acetaminophen. After 10 min of global, low-flow myocardial ischemia, MAP50 and MAP90 (monophasic action potentials at 50 and 90% repolarization, respectively) decreased without acetaminophen (e.g. MAP50, 31+/-4 ms) but did not change during the same time interval with acetaminophen (e.g. MAP50, 57+/-6 ms)(P < 0.05). During ischemia and reperfusion, acetaminophen attenuated the release of hydroxyl radicals and peroxynitrite. Collectively these data reveal cardioprotective, antioxidant behavior of acetaminophen. Under selected conditions (e.g. those causing release of free radicals and other oxidants) such behavior might also prevent ventricular arrhythmias.
G F Merrill; E Goldberg
Related Documents :
1929658 - Captopril, an ace inhibitor, for optimizing reperfusion after acute myocardial infarction.
9706808 - Metabolic modulation of cellular redox potential can improve cardiac recovery from isch...
3978668 - Freeze-thaw injury of rat heart across an intact diaphragm: a new model for the study o...
2513428 - The protection of the acute ischemic myocardium: merits and demerits of the coronary re...
15261178 - Interleukin-6 and b-type natriuretic peptide are independent predictors for worsening o...
23146158 - Repairing chronic myocardial infarction with autologous mesenchymal stem cells engineer...
Publication Detail:
Type:  In Vitro; Journal Article    
Journal Detail:
Title:  Basic research in cardiology     Volume:  96     ISSN:  0300-8428     ISO Abbreviation:  Basic Res. Cardiol.     Publication Date:  2001 Sep 
Date Detail:
Created Date:  2001-10-18     Completed Date:  2002-03-12     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0360342     Medline TA:  Basic Res Cardiol     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  423-30     Citation Subset:  IM    
Department of Cell Biology and Neurosciences, Rutgers University, Piscataway, NJ 08854-8082, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Acetaminophen / pharmacology*
Action Potentials / drug effects
Analgesics, Non-Narcotic / pharmacology*
Antioxidants / pharmacology*
Cardiotonic Agents / pharmacology*
GABA Modulators
Guinea Pigs
Heart Conduction System / drug effects
Hydroxyl Radical / analysis
Myocardial Ischemia / drug therapy*
Myocardium / chemistry
Peroxynitrous Acid / analysis
Ventricular Premature Complexes / chemically induced,  drug therapy
Reg. No./Substance:
0/Analgesics, Non-Narcotic; 0/Antioxidants; 0/Cardiotonic Agents; 0/GABA Modulators; 103-90-2/Acetaminophen; 14691-52-2/Peroxynitrous Acid; 3352-57-6/Hydroxyl Radical; 76-74-4/Pentobarbital

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

Previous Document:  Estimation of the abundance of the cadmium resistance gene cadA in microbial communities in polluted...
Next Document:  Antioxidant changes in the hypertrophied heart due to energy metabolic disorder.