Whole body and splanchnic oxygen consumption and blood flow after oral ingestion of fructose or glucose

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.

1994 ◽  
Vol 266 (3) ◽  
pp. E396-E402 ◽  
Author(s):  
T. Brundin ◽  
J. Wahren

The thermic effect of amino acid administration was examined in healthy subjects. Pulmonary and splanchnic oxygen uptake, cardiac output, splanchnic blood flow, and blood temperatures were measured in eight healthy men before and during 2.5 h of intravenous infusion of 600 kJ of a mixture of 19 amino acids. Indirect calorimetry and catheter techniques were used, including thermometry in arterial and a hepatic venous blood. During the infusion, pulmonary oxygen uptake rose progressively from a basal value of 269 +/- 6 to 321 +/- 8 ml/min after 2.5 h. The splanchnic oxygen consumption increased from a basal level of 64 +/- 4 to a peak value of 91 +/- 7 ml/min after 2 h of infusion. The 2.5 h average splanchnic proportion of the amino acid-induced whole body thermogenesis was 51 +/- 11%. Cardiac output increased from 6.2 +/- 0.3 in the basal state to 7.3 +/- 0.4 l/min, whereas the splanchnic blood flow remained unchanged during the infusion period. The arteriohepatic venous oxygen difference increased from 51 +/- 4 in the basal state to 65 +/- 5 ml/l after 2 h of amino acid infusion. The blood temperature rose by approximately 0.25 degrees C during the amino acid infusion, reflecting an increased heat accumulation in the body. It is concluded that the splanchnic tissues account for approximately one-half of the amino acid-induced whole body thermogenesis, that amino acid infusion augments blood flow in the extrasplanchnic but not in the splanchnic tissues, and stimulates the accumulation of heat in the body most likely via a resetting of the central thermosensors.


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.


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.


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.


1958 ◽  
Vol 193 (1) ◽  
pp. 161-168 ◽  
Author(s):  
Leo A. Sapirstein

K42 Cl, Rb86Cl and iodoantipyrine (I131) were given in single intravenous injections to rats. The isotope content of the organs and the arterial blood concentrations were studied as a function of time. K42Cl and Rb86Cl reached a stable level in all organs other than the brain in 6–9 seconds and maintained this level until 64 seconds. The arterial concentration curves for the isotopes showed that the injected dose was almost completely transferred into the arterial system at about 6–8 seconds. The isotopes showed subsequent recirculation amounting to about 40% of the original dose between the first recirculation and 64 seconds. The organs which displayed stability during the period of recirculation must have had extraction ratios from zero time less than 1.00 but equal to that of the whole body. The fractional uptake of indicator by such organs must therefore have been equal to their blood flow fraction of the cardiac output. The brain reached its maximum content of Rb86 and K42 in 5–6 seconds; both isotopes then disappeared rapidly. The brain was thus shown to have a lower extraction ratio toward these isotopes than the body as a whole; its flow fraction could not therefore be measured by their use. Most organs failed to show stability of their iodoantipyrine content between 9 and 64 seconds; this indicator is not suitable for the measurement of the flow fraction of such organs. By combining values for the cardiac output and the fractional uptake of K42 in dog organs, regional blood flow values were obtained. For those other organs where flow values by other methods are available, the agreement was good. The following blood flow values were obtained in the major organs of the dog: Heart (coronary flow), 1.0 ml/gm/min.; kidney, 3.0 ml/gm/min.; liver, 1.2 ml/gm/min. (0.4 ml/gm/min. hepatic artery, 0.8 ml/gm/min. portal vein); skin, 0.07 ml/gm/min.


1977 ◽  
Vol 43 (2) ◽  
pp. 204-210 ◽  
Author(s):  
A. Capderou ◽  
J. Polianski ◽  
J. Mensch-Dechene ◽  
L. Drouet ◽  
G. Antezana ◽  
...  

An impairment of gluconeogenesis has been proposed to explain the low arterial blood glucose of highlanders. Therefore, we studied splanchnic blood flow, splanchnic uptake of oxygen and lactate, and output of glucose in nine normal and six anemic highlanders at an altitude of 3,750 m. Splanchnic blood flow, arteriovenous difference for oxygen, and oxygen consumption were comparable at rest in both groups and in lowlanders from the literature, whereas splanchnic output of glucose, and uptake of lactate were approximately twice those in lowlanders. After 10 min of mild exercise in 12 subjects (7 normals, 5 anemic), no significant changes in splanchnic hemodynamics and metabolism were found. During 29% oxygen breathing in 8 subjects (5 normals, 3 anemics), arterial lactate, splanchnic uptake of lactate and output of glucose fell to normal sea-level values. We concluded that splanchnic hemodynamics are similar in adapted highlanders and in lowlanders, and that there is no evidence of an impaired gluconeogenesis at the altitude of the present study.


1959 ◽  
Vol 197 (5) ◽  
pp. 1111-1114 ◽  
Author(s):  
Matthew N. Levy

Temperature was diminished in a stepwise fashion in the isolated kidney of the dog perfused from a peripheral artery of the original, normothermic animal. Decreased temperature resulted in an appreciable reduction of renal blood flow at constant arterial blood pressure. Increased blood viscosity and vasoconstriction were both responsible for this reduction of flow. Hypothermia also resulted in a reduction in arteriovenous oxygen difference which was roughly proportional to the centigrade temperature. Furthermore, hypothermia exerted a marked but reversible depression of the rate of oxidative metabolism. This effect was relatively more severe than the changes for the body as a whole at equivalent temperatures reported by other investigators.


1984 ◽  
Vol 62 (7) ◽  
pp. 769-774 ◽  
Author(s):  
C. E. King ◽  
S. M. Cain ◽  
C. K. Chapler

To compare with earlier studies of anemic hypoxia obtained by hemodilution, O2 carring capacity was decreased by carbon monoxide (CO) hypoxia. Arterial O2 content was reduced either 50% (moderate CO) or 65% (severe CO). In two groups of anesthetized dogs (moderate and severe CO) hindlimb innervation remained intact while in a third group (moderate CO) the hindlimb was denervated. Measurements were obtained prior to and at 30 and 60 min of CO hypoxia. Cardiac output was elevated at 30 min of CO hypoxia in all groups (p < 0.01) and in the severe CO group at 60 min (p < 0.01). Hindlimb blood flow remained unchanged during CO hypoxia in the intact groups. In the denervated group, hindlimb blood flow was greater (p < 0.05) than that in the intact groups throughout the experiment. A decrease in mean arterial pressure (p < 0.01) in all groups was associated with a fall in total resistance (p < 0.01). Hindlimb resistance remained unchanged during moderate CO hypoxia in the intact group but increased (p < 0.05) in the denervated group. In the severe CO group hindlimb resistance was decreased (p < 0.05) at 60 min. The results indicate that the increase in cardiac output during CO hypoxia was directed to nonmuscle areas of the body and that intact sympathetic innervation was required to achieve this redistribution.


1986 ◽  
Vol 64 (1) ◽  
pp. 7-12 ◽  
Author(s):  
C. K. Chapler ◽  
S. M. Cain

The mechanisms by which the body attempts to avoid tissue hypoxia when total body oxygen delivery is compromised during acute anemia are reviewed. When the hematocrit is reduced by isovolemic hemodilution the compensatory adjustments include an increase in cardiac output, redistribution of blood flow to some tissues, and an increase in the whole body oxygen extraction ratio. These responses permit whole body oxygen uptake to be maintained until the hematocrit has been lowered to about 10%. Several factors are discussed which contribute to the increase in cardiac output during acute anemia including the reduction in blood viscosity, sympathetic innervation of the heart, and increased venomotor tone. The latter has been shown to be dependent on intact aortic chemoreceptors. With respect to peripheral vascular responses, the rise in coronary and cerebral blood flows which occur following hemodilution is proportionally greater than the increase in cardiac output while the opposite is true for kidney, liver, spleen, and intestine. Skeletal muscle does not contribute to a redistribution of blood flow to more vital areas during acute anemia despite its relatively large anaerobic capacity. Overall, peripheral compensatory adjustments result in an increased oxygen extraction ratio during acute anemia which reflects a better matching of the limited oxygen supply to tissue oxygen demands. However, some areas such as muscle are relatively overperfused which limits an even more efficient utilization of the reduced oxygen supply. Studies of the response of the microcirculation and the extent to which sympathetic vascular controls are involved in peripheral blood flow regulation are necessary to further appreciate the complex pattern of physiological responses which help ensure survival of the organism during acute anemia.


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.


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