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Titolo:
Influence of nitric oxide synthase and adrenergic inhibition on adenosine-induced myocardial hyperemia
Autore:
Buus, NH; Bottcher, M; Hermansen, F; Sander, M; Nielsen, TT; Mulvany, MJ;
Indirizzi:
Aarhus Univ Hosp, Ctr Clin Pharmacol, DK-8000 Aarhus C, Denmark Aarhus Univ Hosp Aarhus Denmark C n Pharmacol, DK-8000 Aarhus C, Denmark Aarhus Univ Hosp, Dept Cardiol, DK-8000 Aarhus, Denmark Aarhus Univ Hosp Aarhus Denmark DK-8000 Cardiol, DK-8000 Aarhus, Denmark Aarhus Univ Hosp, PET Ctr, DK-8000 Aarhus C, Denmark Aarhus Univ Hosp Aarhus Denmark C sp, PET Ctr, DK-8000 Aarhus C, Denmark Univ Copenhagen, Muscle Res Ctr, DK-1168 Copenhagen, Denmark Univ Copenhagen Copenhagen Denmark DK-1168 , DK-1168 Copenhagen, Denmark Univ Aarhus, Dept Pharmacol, DK-8000 Aarhus C, Denmark Univ Aarhus Aarhus Denmark C , Dept Pharmacol, DK-8000 Aarhus C, Denmark
Titolo Testata:
CIRCULATION
fascicolo: 19, volume: 104, anno: 2001,
pagine: 2305 - 2310
SICI:
0009-7322(20011106)104:19<2305:IONOSA>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
CORONARY FLOW RESERVE; BLOOD-FLOW; YOUNG MEN; ARTERIAL-PRESSURE; N-13 AMMONIA; HEART-RATE; HUMANS; VASODILATION; HYPERTENSION; MICROCIRCULATION;
Keywords:
adenosine; nitric oxide; perfusion; receptors, adrenergic, alpha; vasodilation;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Buus, NH Aarhus Univ Hosp, Ctr Clin Pharmacol, Univ Pk 240, DK-8000 AarhusC, Denmark Aarhus Univ Hosp Univ Pk 240 Aarhus Denmark C Aarhus C, Denmark
Citazione:
N.H. Buus et al., "Influence of nitric oxide synthase and adrenergic inhibition on adenosine-induced myocardial hyperemia", CIRCULATION, 104(19), 2001, pp. 2305-2310

Abstract

Background-Myocardial perfusion during adenosine-induced hyperemia is usedboth in clinical diagnosis of coronary heart disease and for scientific investigations of the myocardial microcirculation. The objective of this study was to clarify whether adenosine-induced hyperemia is dependent on endothelial NO production or is influenced by adrenergic mechanisms. Methods and Results-In 12 healthy men, myocardial perfusion was measured with PET in 2 protocols performed in random order, each including 3 perfusion measurements. First, perfusion was measured at rest. Second, either saline or the NO synthase inhibitor N-G-nitro-L-arginine methyl ester (L-NAME, 4mg/kg) was infused, and perfusion during adenosine-induced hyperemia was determined. Last, in both protocols, the a-receptor blocker phentolamine wasinfused, and perfusion during adenosine-induced hyperemia was determined again. Resting perfusion was similar in the 2 protocols (0.69 +/- 0.14 and 0.66 +/- 0.18 mL . min(-1) . g(-1)). L-NAME increased mean arterial blood pressure by 12 +/- 7 mm Hg (P <0.01) and reduced heart rate by 16 +/-7 bpm (P<0.01). Adenosine-induced hyperemia (1.90 +/-0.33 mL . min(-1) . g(-1)) was attenuated by L-NAME (1.50 +/-0.55 mL . min(-1) . g(-1), P <0.01), The addition of phentolantine had no effect on the adenosine-induced hyperemia (2.10 +/-0.34 mL . min(-1) . g(-1), P=NS). In the presence of L-NAME, however, when the adenosine response was attenuated, phentolamine was able to increase hyperemic perfusion (2.05 +/-0.44 mL . min(-1) . g(-1), P <0.05). Conclusions-Inhibit ion of endogenous NO synthesis attenuates myocardial perfusion during adenosine-induced hyperemia, indicating that coronary vasodilation by adenosine is partly endothelium dependent. alpha -Adrenergic blockade has no effect on adenosine-induced hyperemia unless NO synthesis is inhibited.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/10/20 alle ore 23:57:58