Whole body and splanchnic metabolic and circulatory effects of glucose during beta-adrenergic receptor inhibition

1997 ◽  
Vol 272 (4) ◽  
pp. E678-E687 ◽  
Author(s):  
T. Brundin ◽  
A. K. Aksnes ◽  
J. Wahren

The aim of the study was to assess the possible contribution of adrenergic mechanisms to the thermogenic and circulatory effects of glucose ingestion. With the use of indirect calorimetry and arterial, pulmonary arterial, and hepatic venous catheterization, whole body and splanchnic oxygen uptake and blood flow were examined in nine propranolol-treated healthy male volunteers before and during 2 h after oral ingestion of 75 g of glucose. The glucose effects were compared with those in nine untreated controls. After propranolol, the glucose-induced rise in splanchnic blood flow was reduced by approximately 60%, and the hepatic venous glucose release to the systemic circulation was significantly delayed. Glucose-induced increments in pulmonary and splanchnic oxygen uptake and cardiac output were similar in the two groups. It is concluded that adrenergic mechanisms contribute to the glucose-induced rise in splanchnic blood flow and thereby probably to the time course for intestinal absorption of nutrients. It is suggested that the magnitude of glucose-induced thermogenesis is independent of adrenergic stimulation.

1996 ◽  
Vol 271 (3) ◽  
pp. E496-E504 ◽  
Author(s):  
T. Brundin ◽  
R. Branstrom ◽  
J. Wahren

The metabolic and circulatory responses to intravenous or oral administration of glucose (75 g) were studied in healthy subjects. Pulmonary oxygen uptake increased promptly after oral but not during intravenous glucose infusion. The average 2-h rise above basal in whole body oxygen uptake was 8 +/- 1% (P < 0.001) after oral glucose and 3 +/- 1% (P < 0.05) during intravenous glucose infusion. After oral glucose, splanchnic oxygen uptake rose initially by approximately 15% (P < 0.01) and then declined; its average 2-h postprandial level was not significantly higher than that in the basal state. During intravenous glucose, splanchnic oxygen uptake decreased gradually during the first 75 min, reaching a level approximately 25% below basal (P < 0.05). Oxygen consumption by extrasplanchnic tissues rose significantly and to a similar extent (8%, 2 h average) with both intravenous and oral glucose. Splanchnic blood flow increased significantly after oral but not during intravenous glucose. It is concluded that 1) intravenous infusion and oral glucose administration elicit extrasplanchnic thermogenic effects of similar magnitude, 2) during intravenous glucose infusion, the extrasplanchnic thermogenic effect is counterbalanced by a simultaneous reduction in splanchnic oxygen uptake, resulting in a minimal (3%) net rise in whole body oxygen uptake, and 3) oral glucose ingestion but not intravenous glucose infusion increases the splanchnic blood flow.


1993 ◽  
Vol 264 (4) ◽  
pp. E504-E513 ◽  
Author(s):  
T. Brundin ◽  
J. Wahren

The contribution of the splanchnic tissues to the initial 2-h rise in whole body energy expenditure after ingestion of glucose or fructose was examined in healthy subjects. Indirect calorimetry and catheter techniques were employed to determine pulmonary gas exchange, cardiac output, splanchnic blood flow, splanchnic oxygen uptake, and blood temperatures before and for 2 h after ingestion of 75 g of either fructose or glucose in water solution or of water only. Fructose ingestion was found to increase total oxygen uptake by an average of 9.5% above basal levels; the corresponding increase for glucose was 8.8% and for water only 2.5%. The respiratory exchange ratio increased from 0.84 in the basal state to 0.97 at 45 min after fructose ingestion and rose gradually after glucose to 0.86 after 120 min. The average 2-h thermic effect, expressed as percent of ingested energy, was 5.0% for fructose and 3.7% for glucose (not significant). Splanchnic oxygen consumption did not increase measurably after ingestion of either fructose or glucose. The arterial concentration of lactate rose, arterial pH fell, and PCO2 remained essentially unchanged after fructose ingestion. Glucose, but not fructose, elicited increases in cardiac output (28%) and splanchnic blood flow (56%). Fructose, but not glucose, increased arterial blood temperature significantly. It is concluded that both fructose and glucose-induced thermogenesis occurs exclusively in extrasplanchnic tissues. Compared with glucose, fructose ingestion is accompanied by a more marked rise in CO2 production, possibly reflecting an increased extrasplanchnic oxidation of lactate and an accumulation of heat in the body.


1995 ◽  
Vol 88 (5) ◽  
pp. 543-550 ◽  
Author(s):  
Lene Simonsen ◽  
Camilla Ryge ◽  
Jens Bülow

1. Fourteen healthy subjects were investigated before and for 4 hours after oral intake of 75 g of glucose (n = 8) or tap water (n = 6). Whole-body energy expenditure was measured by an open-circuit ventilated hood system. Blood samples for determination of oxygen, carbon dioxide, glucose and lactate were taken from an artery, a hepatic vein and a femoral vein. Blood flow in the splanchnic region was measured by constant infusion of Indocyanine Green. Leg blood flow was measured by venous occlusion strain-gauge plethysmography. Oxygen uptake and carbon dioxide output in the splanchnic and leg tissues were calculated as the product of blood flow and arteriovenous differences in oxygen or carbon dioxide concentrations. Net exchanges of glucose and lactate across the splanchnic and leg tissues were calculated as the product of blood flow and arteriovenous differences in whole-blood glucose or lactate concentrations. 2. Splanchnic oxygen uptake had a biphasic course with an initial increase from 2.35 ± 0.88 (SD) mmol/min to 2.85 ± 1.20 mmol/min 30 min after the glucose intake (P < 0.005) and a later decrease below the basal value to around 2.02 mmol/min 90–180 min after the glucose intake (P < 0.05). The integrated increase in the splanchnic oxygen uptake during the 4 h after the glucose intake was −32.6 ± 49.7 mmol/240 min. Leg oxygen uptake increased from 4.3 ± 1.4 μmol min−1 100 g−1 to 7.0 ± 3.2 μmol min−1 100 g−1 90 min after the glucose intake (P < 0.01). The integrated increase in leg oxygen uptake was 305.1 ± 394.3 μmol 240 min−1 100 g−1. Assuming leg oxygen uptake mainly represents average skeletal muscle, the skeletal muscle mass can explain around 45% of the whole-body glucose-induced thermogenesis. 3. It is concluded that the splanchnic tissues do not contribute to the integrated glucose-induced thermogenesis owing to a biphasic response in oxygen uptake, with an initial increase and a later decrease. Measurements across a leg give the same information as measurements across a forearm with respect to estimation of glucose-induced thermogenesis in skeletal muscle.


1965 ◽  
Vol 209 (3) ◽  
pp. 532-538 ◽  
Author(s):  
Edward F. Banaszak ◽  
John P. Kampine ◽  
Barbara A. Brault ◽  
James J. Smith

The response of the anesthetized dog to single and repeated doses of colloidal carbon gel (CCG) is quite similar to that reported in other mammalian species. At doses less than 30 mg/kg the clearance rate is high and limited only by splanchnic blood flow. At dose levels above 30 mg/kg the phagocytic index (K) approaches a constant. The minimal dose of CCG for assessment of phagocytic capacity was adjudged to be 40 mg/kg. Large doses of CCG (160 mg/kg) and colloidal SiO2 (350 mg/kg) induced a phagocytic depression accompanied by a marked granulocytopenia as well as prompt and delayed hypotensive reactions. There was a decline of estimated splanchnic blood flow incident to test doses of CCG but no further reduction after an RES-depressing dose of CCG. Colloidal thorium dioxide (4 and 8 ml/kg) did not depress the phagocytic capacity of the canine RES for CCG. It is suggested that the delayed hypotensive reaction may be related to the lesser tolerance to traumatic shock previously reported in RES-depressed animals.


1989 ◽  
Vol 62 (1) ◽  
pp. 23-34 ◽  
Author(s):  
D. G. Burrin ◽  
C. L. Ferrell ◽  
J. H. Eisemann ◽  
R. A. Britton ◽  
J. A. Nienaber

The objective of the present study was to measure changes in splanchnic blood flow and oxygen consumption in sheep fed on a high-concentrate diet ad lib. (ADLIB) or an amount sufficient to maintain body-weight (MAINT) for 21 d. Eleven ram lambs were surgically implanted with chronic indwelling catheters in the portal, hepatic and mesenteric veins and mesenteric artery to measure blood flow and net O2 flux through the liver and portal-drained viscera (PDV). During the 21 d period, PDV (P < 0.05) and liver (P < 0.01) blood flow increased in ADLIB and decreased in MAINT lambs (treatment x day, linear). After 21 d, O2 consumptions in PDV and liver of MAINT lambs were 37 and 63% lower than in ADLIB lambs. In the control period, total splanchnic tissues represented an average of 52% of whole body O2 consumption. After 21 d, the relative contributions of PDV and liver to whole-body O2 consumption were 28 and 41% in ADLIB and 19 and 22% in MAINT lambs respectively. Allometric regression variables indicate that liver O2 consumption responds more rapidly to changes in metabolizable energy intake than portal O2 consumption. These results indicate that blood flow and O2 consumption in both PDV and liver are related to level of nutrition. Furthermore, splanchnic tissues represent a significant component of whole-body O2 consumption that is subject to manipulation by level of nutrition.


1983 ◽  
Vol 61 (2) ◽  
pp. 178-182 ◽  
Author(s):  
C. K. Chapler ◽  
S. M. Cain

The metabolic and cardiovascular adjustments of the whole body and skeletal muscle were studied during moderate and severe acute anemia. In 15 anesthetized dogs, venous outflow from the gastrocnemius–plantaris muscle group was isolated. Cardiac output [Formula: see text], muscle blood flow [Formula: see text], total body and muscle oxygen uptake [Formula: see text] were determined during a control period, and at 30 and 60 min of either (i) moderate anemia (n = 8) in which the mean hematocrit (Hct) was 25% or (ii) progressive anemia (n = 7) in which the mean Hct values were 25% at 30 min and 16% at 60 min of anemia. Muscle [Formula: see text], [Formula: see text], and [Formula: see text] were increased in both groups at 30 min of anemia. By 60 min, [Formula: see text] and [Formula: see text] declined to preanemic control values in the moderate anemia group; whole body [Formula: see text] was maintained at the control level. Arterial oxygen transport was the same in the two groups at both 30 and 60 min of anemia despite the difference in Hct at 60 min. Muscle [Formula: see text] showed a further and similar rise in both groups between 30 and 60 min of anemia. These data show that the rise in muscle [Formula: see text] during acute anemia was not directly proportional to the degree of the hematocrit reduction. Further, the findings suggest that the muscle [Formula: see text] response was related to the decrease in arterial oxygen transport.


1994 ◽  
Vol 267 (5) ◽  
pp. E648-E655 ◽  
Author(s):  
T. Brundin ◽  
J. Wahren

The renal contribution to the amino acid-induced whole body thermogenesis was examined. Using indirect calorimetry and catheter techniques, pulmonary and renal oxygen uptake and blood flow, blood temperatures, and net renal exchange of amino acids, glucose and lactate were measured in eight healthy men before and during 3 h of intravenous infusion of 720 kJ of an amino acid solution. During the infusion, the pulmonary oxygen uptake increased from 252 +/- 12 to 310 +/- 8 ml/min, cardiac output increased from 5.9 +/- 0.3 to 6.8 +/- 0.3 l/min, and the arterial blood temperature increased from 36.34 +/- 0.04 to 36.68 +/- 0.07 degrees C. Renal oxygen consumption, heat production, blood flow, and net glucose exchange remained unchanged during the infusion. The net renal uptake of amino acid energy from the blood rose from 2 +/- 2 to 11 +/- 4 W. The total renal energy expenditure was 9-10 W throughout the study period. It is concluded that intravenous amino acid infusion greatly augments the uptake and utilization of amino acids in the kidneys but does not stimulate the renal oxygen consumption, heat production, blood flow, or glucose release.


1995 ◽  
Vol 78 (6) ◽  
pp. 2294-2300 ◽  
Author(s):  
G. Ahlborg ◽  
E. Weitzberg ◽  
J. Lundberg

The aims were to investigate 1) the effects of endothelin-1 (ET-1) during exercise and 2) the influence of exercise on arterial ET-1 levels. Six healthy subjects performed two exercises of 2 h duration at 50% of peak oxygen uptake preceded by intravenous infusion of physiological saline or ET-1 (4 pmol.kg-1.min-1). Blood specimens were taken from arterial and hepatic vein catheters. Arterial ET-1 rose 15-fold during the infusion. Splanchnic blood flow fell after ET-1 and remained lower than in control subjects during exercise (P < 0.001). Splanchnic glucose production was approximately 25% lower compared with control values during the whole exercise period (P < 0.01). Neither heart rate, arterial glucagon, insulin, catecholamines, renin, glucose, lactate, nor glycerol levels differed from control exercise values. The calculated gluconeogenesis from glycerol and lactate did not differ from the control values. ET-1 levels rose approximately twofold in the control exercise (P < 0.01) and in another group of seven subjects performing 1 h of exercise at 70% of peak oxygen uptake (P < 0.001). In conclusion, ET-1 levels increased during exercise without ET-1 administration. In addition, circulating ET-1 has a (direct or indirect) regulatory action on splanchnic blood flow and glucose metabolism during exercise (and possibly under pathophysiological conditions) in humans.


1982 ◽  
Vol 243 (1) ◽  
pp. G1-G9 ◽  
Author(s):  
P. R. Kvietys ◽  
D. N. Granger

Many vasoactive agents are known to alter oxygen uptake by splanchnic organs. Data from the literature indicate that, in general, vasodilators increase, whereas vasoconstrictors decrease oxygen uptake. We compare and contrast the effects of vasoactive agents on oxygen uptake observed in vivo, under constant-flow and free-flow conditions, to those observed in vitro. The discrepancies between the in vivo and in vitro data are discussed relative to the effects of vasoactive agents on blood flow, intraorgan blood flow distribution, the countercurrent exchange of oxygen, capillary exchange capacity, and oxidative metabolism. Changes in blood flow, oxidative metabolism, and capillary density appear to be the major mechanisms by which vasoactive agents alter splanchnic oxygen uptake in vivo. Experimental designs are proposed that may help minimize inconsistencies in the data in future studies.


1990 ◽  
Vol 64 (2) ◽  
pp. 399-411 ◽  
Author(s):  
J. H. Eisemann ◽  
J. A. Nienaber

The effect of feeding v. fasting, on tissue blood flow, oxygen uptake and proportional contributions of the portal drained viscera (PDV), liver (Expts 1 and 2) and hindquarters (HQ; Expt 2) to whole-body O2 uptake were studied in beef steers. The combined techniques of indirect calorimetry and net tissue flux, the latter being the product of arterio-venous concentration difference and blood flow, were used in the experiments. In response to fasting, whole-body O2 consumption decreased as did O2 uptake by all measured tissues except the liver (trend only in Expt 1). Blood flow to all measured tissues decreased during fasting and fractional uptake of O2 decreased in PDV and increased in liver and HQ (Expt 2). Proportional contribution of specific tissues to whole-body O2 uptake changed when animals were switched from the fed to the fasted state. The percentage consumed by PDV decreased from 25.4 to 19.9, by liver increased from 20.5 to 26.4 and by HQ was unchanged (9.6 and 10.5) in Expt 2. These significant responses in Expt 2 were observed as trends in Expt 1. The changes in proportional contribution of tissues to whole-animal O2 uptake reflect the changing metabolic role of specific tissues to lack of food supply. These findings emphasize the central role of the liver in metabolism and indicate that fasting (catabolic) measurements may not reflect the previous fed (anabolic) physiological state.


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