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Titolo:
The role of coenzyme Q(10) in the pathophysiology and therapy of experimental congestive heart failure in the dog
Autore:
Harker-Murray, AK; Tajik, AJ; Ishikura, F; Meyer, D; Burnett, JC; Redfield, MM;
Indirizzi:
Mayo Clin & Mayo Fdn, Div Cardiovasc Dis & Internal Med, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn Rochester MN USA 55905 Med, Rochester, MN 55905 USA
Titolo Testata:
JOURNAL OF CARDIAC FAILURE
fascicolo: 3, volume: 6, anno: 2000,
pagine: 233 - 242
SICI:
1071-9164(200009)6:3<233:TROCQI>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
ATRIAL NATRIURETIC PEPTIDE; MYOCARDIAL BLOOD-FLOW; VENTRICULAR DYSFUNCTION; ITALIAN MULTICENTER; ANGIOTENSIN-II; CARDIOMYOPATHY; TACHYCARDIA; EFFICACY; SAFETY; MECHANISMS;
Keywords:
enzymes; cardiomyopathy; hormones; antioxidant;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Redfield, MM Mayo Clin & Mayo Fdn, Div Cardiovasc Dis & Internal Med, 200 1St St Sw, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn 200 1St St Sw Rochester MN USA 55905 USA
Citazione:
A.K. Harker-Murray et al., "The role of coenzyme Q(10) in the pathophysiology and therapy of experimental congestive heart failure in the dog", J CARD FAIL, 6(3), 2000, pp. 233-242

Abstract

Background: Coenzyme Q(10) (CoQ(10)) is essential for ATP generation and has antioxidant properties. Decreased CoQ(10) levels have been reported in human heart failure (CHF), but it remains unclear if this is a conserved feature of CHF. The objective of the study was to determine if tnchycardia-induced CHF in the dog is associated with reduced CoQ(10) levels. Furthermore,it was hypothesized that CoQ(10) supplementation may improve CHF severity by preventing CoQ(10) deficiency (if present) or via antioxidant effects. Methods and Results: Serum and myocardial levels of CoQ(10) were examined in normal dogs (n = 6), dogs with CHF (control, n = 5), and dogs with CHF treated with CoQ(10) (CoQ(10); 10 mg/kg/day, n = 5). Serum CoQ(10) levels did not change with CHF in control dogs, and myocardial levels were similar to those of normal dogs. CoQ(10) therapy increased serum but not myocardial levels of CoQ(10). In early CHF, CoQ(10)-treated dogs had lower filling pressures, and, in severe CHF, CoQ(10)-treated dogs had less hypertrophy as compared with untreated dogs. Other indices of CHF severity were similar in control and CoQ(10)-treated dogs. Conclusion: These data indicate that CoQ(10) deficiency is not present in this model of CHF. Although dramatic effects on hemodynamics were not observed, CoQ(10) supplementation did appear to attenuate the hypertrophic response associated with CHF.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/09/20 alle ore 11:38:18