Comparison of hemodynamic and sympathoneural responses to adenosine and lower body negative pressure in man

Rongen, Gerard A.; Senn, Beverley L.; Ando, Shin-ichi; Notarius, Catherine F.; Stone, J A; Floras, John S.

doi:10.1139/y97-005

Cited by 14 publications

(14 citation statements)

References 38 publications

(26 reference statements)

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“…Through several indirect mechanisms, however, adenosine may increase sympathetic activity, for example as a result of activation of chemoreceptors. 13 Furthermore, the adenosine-induced increase in heart rate is known to be accompanied by skeletal muscle sympathetic activity. 12 Such an adenosine-induced increase in sympathetic nervous activity might be particularly marked with the large dose of adenosine used in our study.…”

Section: Discussionmentioning

confidence: 99%

“…9 In humans, forearm plethysmographic studies have reached divergent results regarding the role of NO in adenosine-induced vasodilation. 10,11 The heterogeneity of results may be due to any effects of NO being counteracted by a widespread sympathetic activation caused by adenosine, 12,13 which could be of particular importance in the coronary circulation because of the abundance of coronary ␣-receptors in coronary arterioles. 8,14 Under normal physiological conditions, ␣-adrenergic vasoconstriction in the heart is suppressed by myogenic or metabolic factors.…”

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confidence: 99%

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Influence of Nitric Oxide Synthase and Adrenergic Inhibition on Adenosine-Induced Myocardial Hyperemia

et al. 2001

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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. 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 ␣-receptor blocker phentolamine was infused, and perfusion during adenosine-induced hyperemia was determined again. Resting perfusion was similar in the 2 protocols (0.69Ϯ0.14 and 0.66Ϯ0.18 mL · min Ϫ1 · g Ϫ1 ). L-NAME increased mean arterial blood pressure by 12Ϯ7 mm Hg (PϽ0.01) and reduced heart rate by 16Ϯ7 bpm (PϽ0.01). Adenosine-induced hyperemia (1.90Ϯ0.33 mL · min Ϫ1 · g

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Influence of Nitric Oxide Synthase and Adrenergic Inhibition on Adenosine-Induced Myocardial Hyperemia

et al. 2001

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“…Multi-unit recordings of post-ganglionic MSNA were obtained with a unipolar tungsten electrode inserted selectively into a muscle-nerve fascicle of the right or left peroneal nerve, posterior to the fibular head, as described previously [32]. Acceptable recordings met the following four criteria : (1) spontaneous bursts of neural discharge synchronous with the heart rate ; (2) no response to arousal stimuli or skin stroking ; (3) an increase in nerve burst frequency with apnoea ; (4) a signal to noise ratio of 3 : 1.…”

Section: Sympathetic Nerve Recordingsmentioning

confidence: 99%

Dissociation between microneurographic and heart rate variability estimates of sympathetic tone in normal subjects and patients with heart failure

et al. 1999

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The concept that spectral analysis of heart rate variability (HRV) can estimate cardiac sympathetic nerve traffic in subjects with both normal and impaired left ventricular systolic function has not been validated against muscle sympathetic nerve activity (MSNA). We used coarse-graining spectral analysis to quantify the harmonic and non-harmonic, or fractal, components of HRV and to determine low-frequency (0.0-0.15 Hz; PL) and high-frequency (0.15-0.5Hz; PH) harmonic power. To test the hypothesis that MSNA and HRV representations of sympathetic nerve activity (PL and PL/PH) increase in parallel in heart failure, we recorded heart rate and MSNA during supine rest in 35 patients (age 52.4+/-2 years; mean+/-S. E.M.), with a mean left ventricular ejection fraction of 22+/-2%, and in 34 age-matched normal subjects. Power density was log10 transformed. Mean MSNA was 52.9+/-2.6 bursts/min in heart failure patients and 34.9+/-1.9 bursts/min in normal subjects (P<0.0001). In normal subjects, but not in heart failure patients, total power (PT) (r=-0.41; P=0.02) and fractal power (PF) (r=-0.36; P=0.04) were inversely related to age. In heart failure patients, total and fractal power were reduced (P<0.009 for both), and were inversely related to MSNA burst frequency (r=-0.55, P=0.001 and r=-0.60, P=0. 0003 respectively). In normal subjects, there was no relationship between MSNA and either PL or PH. In heart failure patients, as anticipated, PH was inversely related to MSNA (r=-0.41; P<0.02). However, PL was also inversely rather than directly related to MSNA (r=0.44 for 1/log10 PL; P<0.01). There was no relationship between other sympathetic (PL/PH) or parasympathetic (PH/PT) indices and MSNA in either heart failure patients or normal subjects. The lack of concordance between these direct and indirect estimates of sympathetic nervous system activity indicates that this component of HRV cannot be used for between-subject comparisons of central sympathetic nervous outflow. It is the absence of low-frequency power that relates most closely to sympathetic activation in heart failure.

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“…Adenosine can act directly on the sinus node to reduce heart rate and slow conduction within the atrial-ventricular node [2]. However, when infused intravenously into conscious humans, to achieve lower plasma concentrations, adenosine increases both heart rate and sympathetic nerve traffic to muscle [3,4]. However, when infused intravenously into conscious humans, to achieve lower plasma concentrations, adenosine increases both heart rate and sympathetic nerve traffic to muscle [3,4].…”

Section: Introductionmentioning

confidence: 99%

“…These properties are the basis for one clinical application of adenosine, namely the interruption of supraventricular tachycardia by bolus injection. There are two stimuli to this activation of the sympathetic nervous system : peripheral vasodilation, which reduces baroreceptor afferent nerve discharge, and a receptor-specific sympatho-excitatory reflex elicited by stimulating afferent nerve endings in the carotid body, skeletal muscle, heart and kidney [4][5][6][7][8][9][10]. There are two stimuli to this activation of the sympathetic nervous system : peripheral vasodilation, which reduces baroreceptor afferent nerve discharge, and a receptor-specific sympatho-excitatory reflex elicited by stimulating afferent nerve endings in the carotid body, skeletal muscle, heart and kidney [4][5][6][7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Effect of adenosine on heart rate variability in humans

et al. 1999

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By stimulating afferent nerve endings in skeletal muscle, heart, kidney and the carotid body, adenosine infusion evokes a receptor-specific sympatho-excitatory reflex in humans that overrides its direct negative chronotropic effect. We tested the hypothesis that adenosine increases heart rate by suppressing parasympathetic and augmenting sympathetic components of heart rate variability. High-frequency (PH; 0.15-0.50 Hz) and low-frequency (PL; 0.05-0.15 Hz) components of heart rate variability total power (PT) were determined by spectral analysis. The ratios PH/PT and PL/PH respectively were used to estimate parasympathetic and sympathetic input to the sino-atrial node. Heart rate was recorded before and during a 5 min intravenous infusion of adenosine (140 micrograms.min-1.kg-1) in seven healthy men. Adenosine did not affect blood pressure, but increased heart rate by 33+/-6 beats/min, and reduced PT, PH, PL and PH/PT. In contrast, there was an increase in PL/PH. In a second experiment in nine men, brachial artery infusion of adenosine (15 micrograms.min-1.100 ml-1 forearm tissue) increased heart rate by 3 beats/min, had no effect on PT, PH, PL or PH/PT, yet increased PL/PH. Intra-arterial adenosine exerts a modest effect on heart rate by modulating cardiac sympathetic indices, without affecting parasympathetic indices, of heart rate variability, whereas intravenous infusion of adenosine reduces heart rate variability and raises heart rate by decreasing parasympathetic and increasing cardiac sympathetic tone. These reflex effects may become clinically relevant during adenosine stress testing, or when endogenous adenosine is increased, such as during ischaemia, exercise or vasodepressor reactions, or in heart failure.

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Comparison of hemodynamic and sympathoneural responses to adenosine and lower body negative pressure in man

Cited by 14 publications

References 38 publications

Influence of Nitric Oxide Synthase and Adrenergic Inhibition on Adenosine-Induced Myocardial Hyperemia

Influence of Nitric Oxide Synthase and Adrenergic Inhibition on Adenosine-Induced Myocardial Hyperemia

Dissociation between microneurographic and heart rate variability estimates of sympathetic tone in normal subjects and patients with heart failure

Effect of adenosine on heart rate variability in humans

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