Control of the forearm microcirculation: interactions with measures of obesity and noradrenaline kinetics

1998 ◽  
Vol 95 (2) ◽  
pp. 203-212 ◽  
Author(s):  
Paul J. NESTEL ◽  
Takeshi YAMASHITA ◽  
Takayuki SASAHARA ◽  
Jaye P. F. CHIN-DUSTING ◽  
Murray D. ESLER ◽  
...  

1.Obesity influences the responsiveness of the microcirculation; constriction is augmented probably reflecting heightened sympathetic nervous activity. 2.The responsiveness of the microcirculation in the forearm to constriction and dilation was therefore examined in 14 men and women with varying degrees of abdominal adiposity, to determine the potential effects of sympathetic nervous activity and adiposity on flow. Changes in basal blood flow were measured by venous occlusion plethysmography during intra-arterial infusions of noradrenaline, acetylcholine and sodium nitroprusside and after temporary ischaemia. Total body noradrenaline spillover was also measured, as an index of sympathetic neuronal activity. 3.Parameters of obesity were found to influence the responsiveness of the microcirculation. Changes in vascular resistance with noradrenaline (100 ;ng/min) were positively correlated with body weight, body mass index and waist circumference (r = 0.63, P = 0.02), whereas waist circumference was negatively correlated with post-ischaemia vasodilatation (r = -0.76, P = 0.002). Acetylcholine-induced vasodilatation was inversely related to body mass index (r = -0.53, P = 0.053). 4.Basal blood flow did not correlate with adiposity. Furthermore, vasodilatation with 800 ;ng/min sodium nitroprusside was inversely correlated with total body noradrenaline spillover (r = -0.77, P< 0.001); and changes in flows with noradrenaline (constriction) and post-ischaemia (dilation) were inversely related (r = -0.56, P = 0.035). 5.These findings, taken together, are consistent with increased local sympathetic neuronal responsiveness and diminished nitric-oxide-mediated dilation in the forearm vasculature with increasing body adiposity.

Medicine ◽  
2017 ◽  
Vol 96 (39) ◽  
pp. e8126 ◽  
Author(s):  
Yiu-Hua Cheng ◽  
Yu-Chung Tsao ◽  
I-Shiang Tzeng ◽  
Hai-Hua Chuang ◽  
Wen-Cheng Li ◽  
...  

1989 ◽  
Vol 257 (6) ◽  
pp. H1812-H1818 ◽  
Author(s):  
G. K. Savard ◽  
E. A. Richter ◽  
S. Strange ◽  
B. Kiens ◽  
N. J. Christensen ◽  
...  

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.


1981 ◽  
Vol 1 (s1) ◽  
pp. 71-75 ◽  
Author(s):  
Helmer Ring-Larsen ◽  
Jens H. Henriksen ◽  
Birger Hesse ◽  
Niels Juel Christensen

1972 ◽  
Vol 27 (1) ◽  
pp. 1-6 ◽  
Author(s):  
A. M. Harper ◽  
V. D. Deshmukh ◽  
J. O. Rowan ◽  
W. B. Jennett

1991 ◽  
Vol 261 (5) ◽  
pp. H1659-H1664 ◽  
Author(s):  
U. Leuenberger ◽  
K. Gleeson ◽  
K. Wroblewski ◽  
S. Prophet ◽  
R. Zelis ◽  
...  

Acute hypoxemia leads to activation of the sympathetic nervous system (SNS), yet adrenergic vasoconstriction does not occur and venous plasma norepinephrine (NE) fails to rise as expected. To examine whether this dissociation between SNS tone and plasma NE is due to altered metabolism of NE, we measured arterial NE kinetics ([3H]NE infusion technique) and sympathetic nervous outflow to muscle (peroneal microneurography) during 25-30 min of hypoxemia (spontaneous breathing, mean O2 saturation 74%) in six healthy young men. During hypoxemia, muscle sympathetic nervous activity (MSNA) rose significantly from 12.2 +/- 3.3 to 18.6 +/- 3.5 bursts/min, and the total amplitude increased from 123 +/- 36 to 255 +/- 50 mm/min. NE spillover, an index of NE release at the sympathetic nerve terminals, rose from 1.66 +/- 0.30 to 2.33 +/- 0.40 nmol.min-1.m-2 (P = 0.014). However, NE clearance increased also from 0.99 +/- 0.05 to 1.19 +/- 0.11 l.min-1.m-2 (P = 0.014), and arterial NE rose from 281 +/- 50 to 339 +/- 64 pg/ml (P = 0.023). Hypoxemia resulted in a significant rise in forearm blood flow and a decrease in forearm vascular resistance. The fact that skin blood flow and vascular resistance did not change implies that forearm vasodilation was localized to skeletal muscle. Our results suggest that during acute hypoxemia in humans the SNS is activated but the rise in plasma NE is attenuated because NE clearance is increased.


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