Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2003-11-4
pubmed:abstractText
Neurohormonal activation has been shown to be a major factor in congestive heart failure progression and mortality. The beneficial effects obtained in clinical trials with angiotensin converting enzyme (ACE) inhibitors, beta-blockers and aldosterone antagonists have confirmed this hypothesis. 5,6-Diisobutirroyloxy-2-methyl-aminotetraline hydrochloride (nolomirole) is a selective agonist of prejunctional D(2)-dopaminergic and alpha(2)-adrenergic receptors. The stimulation of these receptors inhibits catecholamine release from sympathetic nerve endings. To confirm that this mechanism can be useful in congestive heart failure, we studied the effects of nolomirole on monocrotaline-induced congestive heart failure. The ACE inhibitor trandolapril was used as reference compound. Rats were given single intraperitoneal injection of either saline (control group; n=20) or monocrotaline (50 mg kg(-1)). Three days later, the monocrotaline-treated animals were randomly allocated (n=50 per group) to oral treatment with distilled water (vehicle group), nolomirole (0.25 mg kg(-1)) twice a day, or trandolapril (0.3 mg kg(-1)) once a day up to sacrifice. On the fourth week after monocrotaline injection, animals with signs of congestive heart failure were sacrificed for evaluation of heart hypertrophy and neuroendocrine alterations. Atrial natriuretic peptide (ANP) and alderosterone were determined by radioimmunoassay in plasma. Tissue norepinephrine concentration was quantified by high-pressure liquid chromatography. Nolomirole and trandolapril significantly reduced (a) hypertrophy of right atria and ventricles, (b) plasma levels of ANP and presence of pleural/peritoneal effusions and (c) norepinephrine depletion of right ventricle. These findings confirmed that nolomirole, like trandolapril, is able to attenuate the heart failure signs in the monocrotaline-induced congestive heart failure model.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1043-6618
pubmed:author
pubmed:issnType
Print
pubmed:volume
49
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1-5
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:14597145-Administration, Oral, pubmed-meshheading:14597145-Adrenergic alpha-Agonists, pubmed-meshheading:14597145-Aldosterone, pubmed-meshheading:14597145-Animals, pubmed-meshheading:14597145-Ascitic Fluid, pubmed-meshheading:14597145-Atrial Natriuretic Factor, pubmed-meshheading:14597145-Body Weight, pubmed-meshheading:14597145-Disease Models, Animal, pubmed-meshheading:14597145-Dopamine Agonists, pubmed-meshheading:14597145-Drug Evaluation, Preclinical, pubmed-meshheading:14597145-Esters, pubmed-meshheading:14597145-Female, pubmed-meshheading:14597145-Heart Atria, pubmed-meshheading:14597145-Heart Failure, pubmed-meshheading:14597145-Heart Ventricles, pubmed-meshheading:14597145-Hypertrophy, Right Ventricular, pubmed-meshheading:14597145-Indoles, pubmed-meshheading:14597145-Monocrotaline, pubmed-meshheading:14597145-Norepinephrine, pubmed-meshheading:14597145-Pleural Effusion, pubmed-meshheading:14597145-Rats, pubmed-meshheading:14597145-Rats, Sprague-Dawley, pubmed-meshheading:14597145-Tetrahydronaphthalenes
pubmed:year
2004
pubmed:articleTitle
Effect of nolomirole on monocrotaline-induced heart failure.
pubmed:affiliation
Laboratory of Cardiovascular Physiopathology, Fondazione S. Maugeri, Via Pindololo 23, 25064 Brescia, Gussago, Italy. evpasini@libero.it
pubmed:publicationType
Journal Article, Comparative Study