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Influence of nitric oxide synthase and adrenergic inhibition on adenosine-induced myocardial hyperemia.
- Source :
-
Circulation [Circulation] 2001 Nov 06; Vol. 104 (19), pp. 2305-10. - Publication Year :
- 2001
-
Abstract
- Background: Myocardial perfusion during adenosine-induced hyperemia is used both 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.<br />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, 4 mg/kg) was infused, and perfusion during adenosine-induced hyperemia was determined. Last, in both protocols, the alpha-receptor blocker phentolamine was infused, 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 phentolamine 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).<br />Conclusions: Inhibition 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.
- Subjects :
- Adult
Arginine pharmacology
Blood Pressure drug effects
Coronary Circulation drug effects
Coronary Circulation physiology
Coronary Vessels diagnostic imaging
Coronary Vessels drug effects
Coronary Vessels physiology
Endothelium, Vascular drug effects
Endothelium, Vascular metabolism
Enzyme Inhibitors pharmacology
Heart physiology
Heart Rate drug effects
Humans
Hyperemia metabolism
Male
Microcirculation drug effects
Microcirculation physiology
Myocardium metabolism
NG-Nitroarginine Methyl Ester pharmacology
Nitric Oxide biosynthesis
Phentolamine pharmacology
Tomography, Emission-Computed
Vascular Resistance drug effects
Vasodilation drug effects
Adenosine pharmacology
Adrenergic alpha-Antagonists pharmacology
Heart drug effects
Hyperemia chemically induced
Nitric Oxide Synthase antagonists & inhibitors
Subjects
Details
- Language :
- English
- ISSN :
- 1524-4539
- Volume :
- 104
- Issue :
- 19
- Database :
- MEDLINE
- Journal :
- Circulation
- Publication Type :
- Academic Journal
- Accession number :
- 11696470
- Full Text :
- https://doi.org/10.1161/hc4401.098293