Haemodynamic and Metabolic Effects of Infused Adenosine in Man

1990 ◽  
Vol 79 (2) ◽  
pp. 131-138 ◽  
Author(s):  
Anders Edlund ◽  
Alf Sollevi ◽  
Birgitta Linde

1. Haemodynamic and metabolic effects of intravenous infusion of adenosine, an endogenous vasodilator, were studied in healthy humans. 2. Catheters were inserted into pulmonary and brachial arteries and into the hepatic and subclavian veins. Cardiac output was determined according to the Fick principle, and splanchnic blood flow was measured by using extraction of Indocyanine Green. Skin blood flow was estimated by a laser Doppler technique, calf blood flow by venous occlusion plethysmography and skeletal muscle and adipose tissue blood flow by a local isotope clearance technique. 3. Adenosine (infused in steps from 40 to 80 μg min−-1 kg−-1 into a central vein) elicited a gradual reduction in the peripheral vascular resistance to less than 50% of the basal level. There was a slight increase in the systemic blood pressure, but the pulmonary arterial and the ventricular filling pressures were unchanged. Cardiac output was doubled, accomplished by a combination of a positive chronotropic effect and an increase in stroke volume, which may be secondary to diminished peripheral resistance. 4. Skin blood flow increased by 100% at 50 μg of adenosine min−-1 kg−-1, whereas splanchnic blood flow rose significantly at 60 μg of adenosine min−-1 kg−-1. Blood flow in the calf, gastrocnemius muscle and adipose tissue did not change significantly. 5. Arterial concentrations of noradrenaline and adrenaline increased by 62 and 43%, respectively, during infusion of adenosine. Arterial levels of glycerol were depressed by more than 50%, but those of glucose and pyruvate were unchanged. 6. In conclusion, exogenous adenosine caused a marked systemic vasodilatation, with different responsiveness in the investigated vascular beds. The vasodilatation occurred in the presence of an increase in generalized sympathetic activity. Adipose tissue blood flow was unaltered despite a considerable reduction in fat mobilization.

1995 ◽  
Vol 269 (6) ◽  
pp. E1059-E1066 ◽  
Author(s):  
B. Stallknecht ◽  
L. Simonsen ◽  
J. Bulow ◽  
J. Vinten ◽  
H. Galbo

Trained humans (Tr) have a higher fat oxidation during submaximal physical work than sedentary humans (Sed). To investigate whether this reflects a higher adipose tissue lipolytic sensitivity to catecholamines, we infused epinephrine (0.3 nmol.kg-1.min-1) for 65 min in six athletes and six sedentary young men. Glycerol was measured in arterial blood, and intercellular glycerol concentrations in abdominal subcutaneous adipose tissue were measured by microdialysis. Adipose tissue blood flow was measured by 133Xe-washout technique. From these measurements adipose tissue lipolysis was calculated. During epinephrine infusion intercellular glycerol concentrations were lower, but adipose tissue blood flow was higher in trained compared with sedentary subjects (P < 0.05). Glycerol output from subcutaneous tissue (Tr: 604 +/- 322 nmol.100 g-1.min-1; Sed: 689 +/- 203; mean +/- SD) as well as arterial glycerol concentrations (Tr: 129 +/- 36 microM; Sed: 119 +/- 56) did not differ between groups. It is concluded that in intact subcutaneous adipose tissue epinephrine-stimulated blood flow is enhanced, whereas lipolytic sensitivity to epinephrine is the same in trained compared with untrained subjects.


1989 ◽  
Vol 257 (4) ◽  
pp. R711-R716 ◽  
Author(s):  
D. B. West ◽  
W. A. Prinz ◽  
M. R. Greenwood

Adipose tissue blood flow was measured in five depots, and plasma concentrations of glucose, insulin, and triglyceride were measured at 0, 15, 30, and 45 min after the start of a meal in unanesthetized, freely moving rats. In addition, adipose tissue lipoprotein lipase activity was measured in four depots before and 45 min after the start of a meal. Plasma glucose was significantly elevated only at the 15-min time point, and while plasma triglyceride increased these changes did not reach significance. Plasma insulin was significantly elevated at all time points after a meal. Feeding resulted in a consistent decrease of adipose tissue blood flow expressed per gram wet weight of tissue. This decrease was maximal at 30 min after the start of feeding. The decrease in adipose tissue blood flow averaged 45% at 45 min after the start of feeding for the five depots evaluated. Lipoprotein lipase activity significantly increased in the retroperitoneal and mesenteric fat depots at 45 min after the meal start, but did not change in the epididymal or dorsal subcutaneous fat depots. These results suggest that a decrease in adipose tissue blood flow is a normal result of a meal in the rat. The regional specificity of changes in adipose tissue lipoprotein lipase activity supports the concept of regional specificity of function for adipose tissue and suggests that the mesenteric and retroperitoneal depots are particularly important for the storage of triglycerides immediately after a meal.


2012 ◽  
Vol 302 (10) ◽  
pp. E1157-E1170 ◽  
Author(s):  
Richard Sotornik ◽  
Pascal Brassard ◽  
Elizabeth Martin ◽  
Philippe Yale ◽  
André C. Carpentier ◽  
...  

According to Fick's principle, any metabolic or hormonal exchange through a given tissue depends on the product of the blood flow to that tissue and the arteriovenous difference. The proper function of adipose tissue relies on adequate adipose tissue blood flow (ATBF), which determines the influx and efflux of metabolites as well as regulatory endocrine signals. Adequate functioning of adipose tissue in intermediary metabolism requires finely tuned perfusion. Because metabolic and vascular processes are so tightly interconnected, any disruption in one will necessarily impact the other. Although altered ATBF is one consequence of expanding fat tissue, it may also aggravate the negative impacts of obesity on the body's metabolic milieu. This review attempts to summarize the current state of knowledge on adipose tissue vascular bed behavior under physiological conditions and the various factors that contribute to its regulation as well as the possible participation of altered ATBF in the pathophysiology of metabolic syndrome.


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