Document Detail


Activity of a new hydrogen sulfide-releasing aspirin (ACS14) on pathological cardiovascular alterations induced by glutathione depletion in rats.
MedLine Citation:
PMID:  20826133     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We investigated the effects of the hydrogen sulfide (H₂S)-releasing derivatives of aspirin (ACS14) and salicylic acid (ACS21) in a rat model of metabolic syndrome induced by glutathione (GSH) depletion, causing hypertension and other pathological cardiovascular alterations. GSH depletion was induced in normal rats by the GSH-synthase inhibitor buthionine sulfoximine (BSO, 30 mmol/L day for seven days in the drinking water). Systolic blood pressure and heart rate were measured daily by the tail-cuff method, and plasma thromboxane B₂, 6-keto-prostaglandin F(2α), 8-isoprostane, GSH, insulin and glucose were determined at the end of the seven-day BSO schedule. In addition, ischemia/reperfusion-induced myocardial dysfunction and endothelial dysfunction were assayed on isolated heart and aortic rings, respectively. Unlike aspirin and salicylic acid, ACS14 and ACS21 reduced BSO-induced hypertension, also lowering plasma levels of thromboxane B₂, 8-isoprostane and insulin, while GSH remained in the control range. Neither ACS14 nor ACS21 caused gastric lesions. Both restored the endothelial dysfunction observed in aortic rings from BSO-treated rats, and in ischemia/reperfusion experiments they lowered left ventricular end-diastolic pressure, consequently improving the developed pressure and the maximum rise and fall of left ventricular pressure. Together with this improvement of heart mechanics there were reductions in the activity of creatine kinase and lactate dehydrogenase in the cardiac perfusate. This implies that H₂S released by both ACS14 and ACS21 was involved in protecting the heart from ischemia/reperfusion, and significantly limited vascular endothelial dysfunction in aortic tissue and the related hypertension.
Authors:
Giuseppe Rossoni; Barbara Manfredi; Valerio Tazzari; Anna Sparatore; Silvio Trivulzio; Piero Del Soldato; Ferruccio Berti
Related Documents :
9515043 - Ischemic preconditioning: effects on ph, na and ca in newborn rabbit hearts during isch...
8498583 - Albumin-binding superoxide dismutase with a prolonged half-life reduces reperfusion bra...
4830233 - Digitalis-induced increase in aortic regurgitation and the contrasting effect of glucag...
Publication Detail:
Type:  Journal Article     Date:  2010-09-15
Journal Detail:
Title:  European journal of pharmacology     Volume:  648     ISSN:  1879-0712     ISO Abbreviation:  Eur. J. Pharmacol.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-10-12     Completed Date:  2011-01-21     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  1254354     Medline TA:  Eur J Pharmacol     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  139-45     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier B.V. All rights reserved.
Affiliation:
Dipartimento di Farmacologia, Chemioterapia e Tossicologia Medica, University of Milan, Via Vanvitelli 32, 20129 Milan, Italy. giuseppe.rossoni@unimi.it
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Aorta / drug effects,  metabolism,  pathology,  physiopathology
Aspirin / analogs & derivatives,  chemistry*,  pharmacology*,  therapeutic use
Blood Pressure / drug effects
Consciousness
Creatine Kinase / metabolism
Endothelium, Vascular / drug effects,  physiopathology
Gastric Mucosa / drug effects
Glutathione / deficiency*,  metabolism
Heart / drug effects*,  physiopathology
Heart Rate / drug effects
Hydrogen Sulfide / chemistry*
L-Lactate Dehydrogenase / metabolism
Male
Malondialdehyde / metabolism
Metabolic Syndrome X / chemically induced,  drug therapy,  metabolism,  physiopathology
Myocardial Reperfusion Injury / metabolism,  physiopathology
Myocardium / metabolism*
Oxidative Stress / drug effects
Rats
Rats, Wistar
Vasodilation / drug effects
Chemical
Reg. No./Substance:
50-78-2/Aspirin; 542-78-9/Malondialdehyde; 70-18-8/Glutathione; 7783-06-4/Hydrogen Sulfide; EC 1.1.1.27/L-Lactate Dehydrogenase; EC 2.7.3.2/Creatine Kinase

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


Previous Document:  Metabotropic glutamate receptor mGlu2 is resistant to homologous agonist-induced desensitization but...
Next Document:  Chronic lithium treatment protects the rat kidney against ischemia/reperfusion injury: the role of n...