Postprandial Sympatho-Adrenal Activity: Its Relation to Metabolic and Cardiovascular Events and to Changes in Meal Frequency

1995 ◽  
Vol 89 (4) ◽  
pp. 349-357 ◽  
Author(s):  
Mario Vaz ◽  
Andrea Turner ◽  
Bronwyn Kingwell ◽  
Jaye Chin ◽  
Elizabeth Koff ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiovascular Events ◽  
Peak Plasma ◽  
Nervous Activity ◽  
Systolic Pressure ◽  
Plasma Noradrenaline ◽  
Whole Body ◽  
Sympathetic Nervous Activity ◽  
Insulin Levels ◽  
Sympathetic Nervous

1. Sympatho-adrenal activity was measured after the consumption of a 3.15 MJ mixed meal. Whole-body noradrenaline spillover rates, forearm plasma noradrenaline spillover and adrenaline secretion rates were derived using isotope dilution methodology. Heart rate and blood pressure spectral analysis measurements were also made. The relation of sympatho-adrenal activity to thermogenic and cardiovascular events was studied. Sympathetic nervous and thermogenic responses were measured for 120 min after the single 3.15 MJ meal and compared with those after three 1.05 MJ meals, given 30 min apart. 2. Whole-body and forearm plasma noradrenaline spillover, and the 0.1 Hz component of systolic pressure power all increased significantly postprandially, while the 0.1 Hz component of heart rate variability, an indirect index of cardiac sympathetic nervous activity, remained unaltered. Adrenaline secretion was unaltered postprandially. Whole-body plasma noradrenaline spillover and thermogenesis during the 120 min postprandial period were 37% and 36% higher after the single meal as compared with the multiple meals, although this was not statistically significant. 3. The sympathetic neural responses were delayed in relation to peak plasma insulin levels and sustained in the face of declining insulin levels. Energy expenditure increased significantly postprandially, but there was no direct quantitative relationship to plasma noradrenaline spillover. Forearm oxygen consumption did not increase postprandially despite significant increases in regional noradrenaline spillover. Thus, no close relation was demonstrated between postprandial sympathetic nervous activation and either insulin secretion or thermogenesis.

Noradrenaline Kinetics and Coronary Haemodynamics during Acute β1-Adrenoceptor Blockade in Man

1993 ◽  
Vol 84 (4) ◽  
pp. 413-417 ◽  
Author(s):  
Alastair J. McCance ◽  
J. Colin Forfar
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Nervous Activity ◽  
Whole Body ◽  
Sympathetic Nervous Activity ◽  
Coronary Vascular Resistance ◽  
Diagnostic Cardiac Catheterization ◽  
Sympathetic Nervous ◽  
Arterial Plasma ◽  
Coronary Sinus Blood

1. To investigate the effects of acute β1-adrenoceptor blockade on sympathetic nervous activity, cardiac and whole-body noradrenaline kinetics were determined during intravenous infusions of saline placebo and of metoprolol (10-15 mg plus 150 μg min−1 kg−1) in 10 patients undergoing diagnostic cardiac catheterization, in whom β-adrenoceptor antagonists had been discontinued for 7 days. 2. Coronary haemodynamics were measured in these 10 patients plus two others. Compared with saline placebo, metoprolol administration was associated with decreases in heart rate (68 ± 2 to 59 ± 3 beats/min, P < 0.001) and coronary sinus blood flow (86 ± 8 to 68 ± 6 ml/min, P < 0.001) and an increase in calculated coronary vascular resistance (1.42 ± 0.19 to 1.75 ± 0.22 mmHg min ml−1, P < 0.001). Arterial and femoral venous noradrenaline concentrations, whole-body noradrenaline clearance and whole-body noradrenaline spillover to arterial plasma did not change. In contrast, cardiac noradrenaline spillover (33.7 ± 5.1 to 20.2 ± 4.3 pmol/min, P < 0.05) and cardiac noradrenaline clearance (31 ± 3 to 23 ± 3 ml/min, P < 0.001) were significantly decreased during metoprolol administration. 3. These results may be explained by inhibition of pre-junctional facilitatory β-adrenoceptors, which we hypothesize may be predominantly of the β1-subtype in the heart and of the β2-subtype in the periphery.

Variations in Individual Organ Release of Noradrenaline Measured by An Improved Radioenzymatic Technique; Limitations of Peripheral Venous Measurements in the Assessment of Sympathetic Nervous Activity

1981 ◽  
Vol 61 (5) ◽  
pp. 585-590 ◽  
Author(s):  
M. J. Brown ◽  
D. A. Jenner ◽  
D. J. Allison ◽  
C. T. Dollery
Keyword(s):  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Nervous Activity ◽  
Artery Stenosis ◽  
Plasma Noradrenaline ◽  
Sympathetic Nervous Activity ◽  
Release Of Noradrenaline ◽  
Noradrenaline Concentration ◽  
Sympathetic Nervous ◽  
Noradrenaline And Adrenaline

1. The validity of plasma noradrenaline as an index of sympathetic nervous activity was assessed by estimating variation in individual organ contribution to circulating concentrations. 2. Arteriovenous (A—V) differences in noradrenaline and adrenaline concentration were measured across several organs in nine patients with mild essential hypertension, in five with renal artery stenosis and 15 phaeochromocytoma patients. 3. In patients with phaeochromocytomas the percentage extraction of noradrenaline and adrenaline (estimated from the A—V differences) was similar across all organs, suggesting that adrenaline extraction could be used as a marker for noradrenaline extraction. 4. In the non-tumour patients the A—V difference for noradrenaline was less than that for adrenaline across most organs studied, reflecting the net result of noradrenaline release and extraction. The estimated contribution of various organs to the noradrenaline concentrations in their venous effluent was: heart. 21%; kidney 47%; legs 68%. 5. This pattern of A—V difference proved a positive diagnostic feature for non-tumour patients since it was not found even in the patients with small phaeochromocytomas, whose peripheral venous noradrenaline concentration alone did not distinguish them. 6. The venous-arterial difference across the adrenal glands of non-tumour patients was more than 10-fold greater for adrenaline than that for noradrenaline. Since the mean arterial concentration of noradrenaline was more than fivefold higher than that of adrenaline, the normal adrenal contribution to circulating noradrenaline is likely to be less than 2%. 7. In the patients with renal artery stenosis renal venous concentrations of noradrenaline (from the ischaemic kidney) were higher than arterial values, but mean arterial values were no higher than in the essential hypertensive patients. 8. Local variations in sympathetic activity may occur without altering the plasma noradrenaline concentration measured in peripheral plasma.

Heart Rate Variability During Early Mobilization in Patients with Acute Ischemic Stroke

2018 ◽  
Vol 80 (1-2) ◽  
pp. 50-54 ◽  
Author(s):  
Masafumi Nozoe ◽  
Miho Yamamoto ◽  
Miki Kobayashi ◽  
Masashi Kanai ◽  
Hiroki Kubo ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Nervous Activity ◽  
Early Mobilization ◽  
Sympathetic Nervous Activity ◽  
Parasympathetic Nerve ◽  
Significant Difference ◽  
Sympathetic Nervous

Autonomic dysfunction is one of the predictors of poor outcome in patients with acute ischemic stroke. We compared the heart rate variability (HRV) during early mobilization in patients with or without neurological deterioration (ND). We enrolled 7 acute ischemic patients with ND and 14 without ND and measured their HRV in the rest and mobilization by electrocardiography. There was a significant difference in sympathetic nervous activity during mobilization between the 2 groups. However, no significant differences in blood pressure, heart rate, and parasympathetic nerve activity were observed. In patients with acute ischemic stroke, it is likely that the increase in sympathetic nervous activity during mobilization is associated with ND.

Norepinephrine spillover from skeletal muscle during exercise in humans: role of muscle mass

1989 ◽  
Vol 257 (6) ◽  
pp. H1812-H1818 ◽  
Author(s):  
G. K. Savard ◽  
E. A. Richter ◽  
S. Strange ◽  
B. Kiens ◽  
N. J. Christensen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Muscle Mass ◽  
Nervous Activity ◽  
Plasma Concentrations ◽  
Whole Body ◽  
Knee Extensors ◽  
Sympathetic Nervous Activity ◽  
Leg Blood Flow ◽  
Sympathetic Nervous

The purpose of this study was to determine the effect of increasing muscle mass involvement in dynamic exercise on both sympathetic nervous activation and local hemodynamic variables of individual active and inactive skeletal muscle groups. Six male subjects performed 15-min bouts of one-legged knee extension either alone or in combination with the knee extensors of the other leg and/or with the arms. The range of work intensities varied between 24 and 71% (mean) of subjects' maximal aerobic capacity (% VO2max). Leg blood flow, measured in the femoral vein by thermodilution, was determined in both legs. Arterial and venous plasma concentrations of norepinephrine (NE) and epinephrine were analyzed, and the calculated NE spillover was used as an index of sympathetic nervous activity to the limb. NE spillover increased gradually both in the resting, and to a larger extent in the exercising legs, with a steeper rise occurring approximately 70% VO2max. These increases were not associated with any significant changes in leg blood flow or leg vascular conductance at the exercise intensities examined. These results suggest that, as the total active muscle mass increases, the rise in sympathetic nervous activity to skeletal muscle, either resting or working at a constant load, is not associated with any significant neurogenic vasoconstriction and reduction in flow or conductance through the muscle vascular bed, during whole body exercise demanding up to 71% VO2max.

Choice of Control Groups in the Appraisal of Sympathetic Nervous Activity in Essential Hypertension

1979 ◽  
Vol 57 (4) ◽  
pp. 339-344 ◽  
Author(s):  
D. H. Jones ◽  
Carlene A. Hamilton ◽  
J. L. Reid
Keyword(s):  
Essential Hypertension ◽  
Nervous Activity ◽  
Plasma Noradrenaline ◽  
Sympathetic Nervous Activity ◽  
Urinary Catecholamine ◽  
Control Groups ◽  
Laboratory Staff ◽  
Metabolite Concentrations ◽  
Vanillyl Mandelic Acid ◽  
Sympathetic Nervous

1. Plasma noradrenaline concentrations were similar in normotensive and hypertensive outpatients, but were significantly lower in laboratory control subjects. 2. Standing plasma noradrenaline concentrations were similar in all three groups. 3. Urinary vanillyl mandelic acid, catecholamines and metanephrines were also similar in the normotensive and hypertensive groups. 4. Laboratory controls, possibly because of familiarity with the techniques of sphygmomanometry and blood sampling, may attain a ‘basal’ resting level of sympathetic nervous discharge more readily and rapidly than subjects who are unfamiliar with such procedures. 5. After orthostatic stimulation by standing for 2 min, the activity of the sympathetic nervous system, as determined by pulse rate and plasma noradrenaline concentrations, was similar in the three groups, despite the lower starting values in the laboratory staff. 6. The absence of differences in plasma noradrenaline or urinary catecholamine and metabolite concentrations does not support the hypothesis of excessive sympathetic nervous activity in essential hypertension.

Abstract 5430: Obstructive Sleep Apnoea Exacerbates Muscular Sympathetic Nervous Activity in Patients with Metabolic Syndrome

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Ivani C Trombetta ◽  
Cristiane M Nunes ◽  
Luciano F Drager ◽  
Raffael F Fraga ◽  
Maria Janieire N Alves ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Heart Rate ◽  
Oxygen Saturation ◽  
Obstructive Sleep Apnoea ◽  
Nervous Activity ◽  
Sleep Apnoea ◽  
Sympathetic Nervous Activity ◽  
Obstructive Sleep ◽  
Sympathetic Nervous

Obstructive sleep apnoea (OSA) and metabolic syndrome (MetS) independently increases muscular sympathetic nervous activity (MSNA). Unknown is whether OSA has an additive effect on MSNA in patients with MetS. We tested the hypothesis that: OSA would have an additive effect on MSNA in patients with MetS. In addition, we studied whether the increase in MSNA in patients with MetS is associated with alteration in arterial baroreflex sensitivity (BRS). Twenty four patients with MetS diagnosed according ATP-III were divided in two groups: MetS+OSA (n=14) and MetS (n=10). They were matched for age, body mass index, waist circumference, and metabolic profile: OSA was defined by an apnoea/hypopnoea index (AHI)>15 events/hour by polysonography. MSNA was recorded directly from the peroneal nerve using the technique of microneurography. Blood pressure (BP) was monitored on a beat-by-beat basis (Finapress) and heart rate by ECG. BRS was analyzed by spontaneous BP and heart rate fluctuations. AHI was higher (42±9 vs. 7±1 events/h, P =0.0001) and minimum oxygen saturation lower (77±2 vs. 87±1 %, P =0.001) in MetS+OSA patients. Patients MetS+OSA had higher MSNA (55±3 vs. 43±2 bursts/100 beats, P =0.01) and systolic BP (158±4 vs.144±3 mmHg, P =0.01) when compared with patients with MetS without OSA. Further analysis showed that AHI and minimum oxygen saturation have significant correlation with MSNA (r=0.65; P =0.001 and r=−0.48; P =0.017, respectively). Patients with MetS+OSA had lower BRS for increases (7.8±0.9 vs. 13.4 ± 1.4 msec/mmHg, P =0.01) and decreases (7.2±0.9 vs. 13.2 ± 2.0 msec/mmHg, P =0.03) in blood pressure than patients with MetS without OSA. MSNA significantly correlated with BRS during spontaneous increases in blood pressure (r=−0.56, P =0.01). OSA exacerbates MSNA in patients with MetS. In addition, the augmented MSNA in patients with MetS+OSA is associated with reduced BRS. These findings suggest that OSA increases the risk for cardiovascular disease in patients with MetS.

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