Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Increased inactivation of nitric oxide is involved in impaired coronary flow reserve in heart failure
Autore:
Nakamura, R; Egashira, K; Arimura, K; Machida, Y; Ide, T; Tsutsui, H; Shimokawa, H; Takeshita, A;
Indirizzi:
Kyushu Univ, Grad Sch Med, Dept Cardiovasc Med, Fukuoka 8158552, Japan Kyushu Univ Fukuoka Japan 8158552 Cardiovasc Med, Fukuoka 8158552, Japan
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
fascicolo: 6, volume: 281, anno: 2001,
pagine: H2619 - H2625
SICI:
0363-6135(200112)281:6<H2619:IIONOI>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
IDIOPATHIC DILATED CARDIOMYOPATHY; SENSITIVE K+ CHANNELS; ENDOTHELIAL DYSFUNCTION; BLOOD-FLOW; PACING TACHYCARDIA; ADENOSINE; DOGS; SUPEROXIDE; VASODILATION; DIPYRIDAMOLE;
Keywords:
oxygen free radicals; endothelium-derived factors;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Egashira, K Kyushu Univ, Grad Sch Med, Dept Cardiovasc Med, Higashi Ku, 3-1-1 Maidashi, Fukuoka 8128552, Japan Kyushu Univ 3-1-1 Maidashi Fukuoka Japan 8128552 28552, Japan
Citazione:
R. Nakamura et al., "Increased inactivation of nitric oxide is involved in impaired coronary flow reserve in heart failure", AM J P-HEAR, 281(6), 2001, pp. H2619-H2625

Abstract

Recent evidence suggests that increased inactivation of endothelium-derived nitric oxide (NO) by oxygen free radical (OFR) formation is involved in the pathogenesis of endothelial dysfunction in heart failure (HF). However, it is unclear whether increased OFR limits coronary flow reserve in HF. To test this hypothesis, we examined the effects of antioxidant therapy on coronary flow reserve in a canine model of tachycardia-induced HF. The flow reserve (percent increase in coronary blood flow) to adenosine or to 20-s ischemia was less and OFR formation (electron-spin resonance spectroscopy) in myocardial tissues was greater in HF dogs than in controls. Immunohistochemical staining of 4-hydroxy-2-nonenal, an OFR-induced lipid peroxide, was detected in coronary microvessels of HF dogs. Intracoronary infusion of a cell-permeable OFR scavenger, tiron, suppressed OFR formation and improved thevasodilating capacity to adenosine or brief ischemia in HF dogs but not incontrols. A NO synthesis inhibitor, N-G-monomethyl-L-arginine (L-NMMA), diminished the beneficial effects of tiron in HF dogs. Vasodilation to sodiumnitroprusside was similar between control and HF dogs, and no change in its response was noted with tiron or tiron + L-NMMA in either group. In summary, antioxidant treatment with tiron improved coronary flow reserve by increasing NO bioactivity in HF dogs. Thus increased OFR formation may impair coronary flow reserve in HF by reducing NO bioactivity.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 12:02:38