Metabolic responses of the whole body, portal-drained viscera and hindquarter to adrenaline infusion: Effects of nonselective and selective β-adrenoceptor blockade

1997 ◽  
Vol 77 (2) ◽  
pp. 307-316 ◽  
Author(s):  
J. O. O. Miaron ◽  
R. J. Christopherson
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Portal Vein ◽  
Influencing Factor ◽  
External Iliac Artery ◽  
Open Circuit ◽  
Whole Body ◽  
Organ Blood Flow ◽  
Β Blocker ◽  
Β Blockers

Propranolol, a nonselective β-blocker and selective β-blockers (metoprolol a β1-blocker and ICI 118551 a β2-blocker) were used to investigate the β-adrenoceptor-mediated adrenaline-induced increase in whole-body and organ VO2 in five whether sheep. Transit time blood flow probes were chronically implanted on the portal vein and the external iliac artery and sampling catheters were placed in the mesenteric artery, iliac vein and portal vein. Oxygen consumption by the whole body was measured by open circuit calorimetry, and oxygen consumption by the portal-drained viscera and the hindquarter was determined from A-VO2 differences and organ blood flow. Absolute pre-infusion VO2 values for the whole body, portal-drained viscera and hindquarters were 236 ± 7.4, 61 ± 6.0 and 13 ± 3.1 mL min−1 respectively. The mean changes in VO2 in response to infusion were 74 vs. 11, 26, 10 and 12 mL min−1 (SE = 9.1) for whole body; 31 vs. −2, −15, 13 and −4 mL min−1 (SE = 7.3) for portal-drained viscera and 8 vs. −0.4, 2.1, 1.0 and −2.7 mL min−1; SE = 4.3) for hindquarters during adrenaline, control, propranolol, metoprolol and ICI 118551 treatments, respectively. Adrenaline increased VO2 (P < 0.05) in the whole body and portal-drained viscera, but not hindquarters relative to controls. All β-blockers suppressed (P < 0.05) the adrenaline-induced increase in VO2 except for the portal-drained viscera where metoprolol was less effective and the hindquarters where β-blockers had no effect. The blood flow pattern was similar to VO2 responses for the portal-drained viscera. The nonselective β1 and β2 blockers were effective in reducing the adrenaline-induced increases in blood flow from the portal-drained viscera and to the hindquarters, with more pronounced β-adrenoceptor-mediated haemodynamic effects. The results indicate that the β-adrenoceptor system modulates whole body VO2, clearly establishes that adrenaline induces an increased VO2 in portal-drained viscera which can be reversed by a β2 or nonselective β blocker and implicates β adrenoceptors as an influencing factor in the maintenance energy requirements of ruminants. Key words: Calorimetry, adrenaline, β blockers, blood flow, sheep

Metabolic responses of the whole body, portal-drained viscera and hind quarter to acute cold exposure and feeding in sheep: Effects of nonselective and selective β-adrenoceptor blockade

1997 ◽  
Vol 77 (4) ◽  
pp. 707-714 ◽  
Author(s):  
J. O. O. Miaron ◽  
R. J. Christopherson
Keyword(s):  
Oxygen Consumption ◽  
Cold Exposure ◽  
Open Circuit ◽  
Whole Body ◽  
Receptor Subtype ◽  
Concentration Difference ◽  
Adrenoceptor Antagonist ◽  
Acute Cold Exposure ◽  
Β Blocker ◽  
Β Blockers

Two experiments were conducted to study the adrenergic regulation of thermogenesis in sheep during acute cold exposure and feeding. Propranolol, a nonselective β-blocker, metoprolol, a β1-blocker and ICI 118551, a β2-blocker, were used to investigate the β-adrenoceptor mediated whole-body and organ oxygen consumption (VO2). Whole-body oxygen consumption was measured by open circuit calorimetry. Portal-drained viscera and hindquarter oxygen consumption was the product of arterio-venous oxygen concentration difference and blood flow across the respective organs. Acute cold exposure increased (P < 0.05) whole body and hindquarters VO2 by about 60% but, not that of the portal drained viscera. Feeding induced a 41% elevation (P < 0.05) in whole body and a nonsignificant increase in the portal drained viscera VO2. The β-adrenoceptor blockers suppressed the increase in whole body VO2 associated with acute cold exposure but, only the reduction induced by the β2-adrenoceptor antagonist (ICI 118551) was significant (P = 0.02). The response to feeding was not altered by the β-blockers. This study suggests that the β-adrenoceptor system plays a role in modulating whole body but not the portal-drained viscera acute cold-induced thermogenesis, and this modulation of energy expenditure may involve a β2 receptor subtype. Key words: Calorimetry, thermogenesis, cold, feed and sheep

scholarly journals Effect of level of nutrition on splanchnic blood flow and oxygen consumption in sheep

1989 ◽  
Vol 62 (1) ◽  
pp. 23-34 ◽  
Author(s):  
D. G. Burrin ◽  
C. L. Ferrell ◽  
J. H. Eisemann ◽  
R. A. Britton ◽  
J. A. Nienaber
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Control Period ◽  
Metabolizable Energy ◽  
Splanchnic Blood Flow ◽  
Whole Body ◽  
Indwelling Catheters ◽  
Maintain Body Weight ◽  
Ram Lambs ◽  
Metabolizable Energy Intake

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.

Muscle and whole body metabolism after norepinephrine

1994 ◽  
Vol 266 (6) ◽  
pp. E877-E884 ◽  
Author(s):  
A. V. Kurpad ◽  
K. Khan ◽  
A. G. Calder ◽  
M. Elia
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Fatty Acid ◽  
Energy Expenditure ◽  
Indirect Calorimetry ◽  
Whole Body ◽  
Marginal Effect ◽  
Nonesterified Fatty Acids ◽  
Acid Cycle ◽  
Triglyceride Fatty Acid

The effect of an infusion of norepinephrine (0.42 nmol.kg-1.min-1) on energy metabolism in the whole body (using indirect calorimetry and the arteriovenous forearm catheterization techniques in eight healthy young male adults. The activity of the triglyceride-fatty acid cycle, which mainly operates in nonmuscular tissues, was also assessed by measuring glycerol turnover using [2H5]glycerol (to indicate lipolysis) and indirect calorimetry (to indicate net fat oxidation). Norepinephrine increased whole body oxygen consumption by almost 10% (P < 0.01), but the estimated oxygen consumption of muscles tended to decrease. Muscle blood flow (measured by 133Xe) and forearm blood flow (measured by strain-gauge plethysmography) were not significantly affected by norepinephrine, but the rate of uptake of nonesterified fatty acids and beta-hydroxybutyrate increased severalfold (P < 0.05), whereas that of glucose did not. The activity of the triglyceride-fatty acid cycle increased fourfold after norepinephrine administration, having a marginal effect on resting energy expenditure (approximately 1.5%) but accounting for approximately 15% of the increase in whole body energy expenditure. This study provides no evidence that skeletal muscle is an important site for norepinephrine-induced thermogenesis and suggests that an increase in the activity of the triglyceride-fatty acid cycle contributes to the norepinephrine-induced increase in energy expenditure of nonmuscular tissues.

Renal oxygen consumption, thermogenesis, and amino acid utilization during i.v. infusion of amino acids in man

1994 ◽  
Vol 267 (5) ◽  
pp. E648-E655 ◽  
Author(s):  
T. Brundin ◽  
J. Wahren
Keyword(s):  
Amino Acids ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Amino Acid ◽  
Oxygen Uptake ◽  
Heat Production ◽  
Whole Body ◽  
Arterial Blood ◽  
Renal Oxygen Consumption ◽  
Renal Oxygen

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.

scholarly journals Development of an Automated Drug Delivery System for an Ultra-Short-acting β-Blocker, Landiolol, to Stably Reduce Myocardial Oxygen Consumption without Inducing Circulatory Collapse in a Canine Heart Failure Model

2020 ◽  
Author(s):  
Takuya Nishikawa ◽  
Kazunori Uemura ◽  
Yohsuke Hayama ◽  
Toru Kawada ◽  
Keita Saku ◽  
...  
Keyword(s):  
Heart Failure ◽  
Drug Delivery ◽  
Oxygen Consumption ◽  
Drug Delivery System ◽  
Acute Phase ◽  
Delivery System ◽  
Myocardial Oxygen Consumption ◽  
Circulatory Collapse ◽  
Β Blocker ◽  
Β Blockers

Abstract Background: Beta-blockers are well known to reduce myocardial oxygen consumption (MVO2) and improve the prognosis of heart failure (HF) patients. Although the use of β-blockers in the acute phase of HF can be expected to be beneficial, the negative chronotropic and inotropic effects limit their use due to the risk of circulatory collapse (cardiogenic shock, and/or pulmonary congestion). A safe method to administer β-blockers in the acute phase of HF is in great need. In this study, we developed an automated drug delivery system that controls the infusion of landiolol, an ultra-short-acting β-blocker, while preventing circulatory collapse. Method: We designed a system that simultaneously regulates cardiac function and volume status to control haemodynamics. The system monitors arterial pressure (AP), left atrial pressure (PLA), right atrial pressure, and cardiac output. Using negative feedback of haemodynamics, the system controls mean AP and mean PLA by administering landiolol, dextran, and furosemide. We applied the system for 60 min to 5 mongrel dogs with rapid pacing-induced HF, and assessed haemodynamics, MVO2 and lactate.Results: In all dogs, the system successfully adjusted delivery of the drugs resulting in accurate control of mean AP and mean PLA. From 15 to 60 min after the system was activated, median of absolute performance error (index of precision of control) was small for mean AP (median [interquartile range], 2.5 [2.1 – 3.7] %) and mean PLA (4.1 [1.8 – 6.2] %). Although the system decreased mean AP compared to baseline, mean and systolic AP were maintained not lower than 70 and 100 mmHg, respectively, and lactate did not increase. Furthermore, the system significantly decreased PLA and MVO2 (3.6 [3.3 – 4.0] to 2.7 [2.5 – 3.3] ml·min-1·100 g left ventricular weight-1) compared to baseline. Consequently, the automated drug delivery system successfully reduced MVO2 without inducing circulatory collapse.Conclusion: We developed an automated landiolol delivery system that achieved safe administration of landiolol in a canine model of acute HF. The system controlled AP and PLA accurately and stably, and reduced MVO2. With further development for clinical application, the automated drug delivery system may be the key tool to improve management of patients with HF.

Changes in Hemodynamics, Regional Organ Blood Flow, and Tissue Oxygen Consumption Under Isoflurane and Enflurane

1987 ◽  
pp. 87-97
Author(s):  
P. Conzen ◽  
J. Hobbhahn ◽  
A. Goetz ◽  
H. Habazettl ◽  
T. Granetzny ◽  
...  
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Organ Blood Flow ◽  
Tissue Oxygen ◽  
Tissue Oxygen Consumption

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
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Oxygen Uptake ◽  
The Body ◽  
Splanchnic Blood Flow ◽  
Whole Body ◽  
Co2 Production ◽  
Arterial Blood ◽  
Splanchnic Oxygen

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.

scholarly journals Roles of nitric oxide synthase and cyclooxygenase in leg vasodilation and oxygen consumption during prolonged low-intensity exercise in untrained humans

2010 ◽  
Vol 109 (3) ◽  
pp. 768-777 ◽  
Author(s):  
William G. Schrage ◽  
Brad W. Wilkins ◽  
Christopher P. Johnson ◽  
John H. Eisenach ◽  
Jacqueline K. Limberg ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Young Adults ◽  
Oxygen Consumption ◽  
Steady State ◽  
Nitric Oxide Synthase ◽  
Muscle Blood Flow ◽  
Blood Gases ◽  
Whole Body ◽  
Oxide Synthase

The vasodilator signals regulating muscle blood flow during exercise are unclear. We tested the hypothesis that in young adults leg muscle vasodilation during steady-state exercise would be reduced independently by sequential pharmacological inhibition of nitric oxide synthase (NOS) and cyclooxygenase (COX) with NG-nitro-l-arginine methyl ester (l-NAME) and ketorolac, respectively. We tested a second hypothesis that NOS and COX inhibition would increase leg oxygen consumption (V̇o2) based on the reported inhibition of mitochondrial respiration by nitric oxide. In 13 young adults, we measured heart rate (ECG), blood pressure (femoral venous and arterial catheters), blood gases, and venous oxygen saturation (indwelling femoral venous oximeter) during prolonged (25 min) steady-state dynamic knee extension exercise (60 kick/min, 19 W). Leg blood flow (LBF) was determined by Doppler ultrasound of the femoral artery. Whole body V̇o2 was measured, and leg V̇o2 was calculated from blood gases and LBF. Resting intra-arterial infusions of acetylcholine (ACh) and nitroprusside (NTP) tested inhibitor efficacy. Leg vascular conductance (LVC) to ACh was reduced up to 53 ± 4% by l-NAME + ketorolac infusion, and the LVC responses to NTP were unaltered. Exercise increased LVC from 4 ± 1 to 33.1 ± 2 ml·min−1·mmHg−1 and tended to decrease after l-NAME infusion (31 ± 2 ml·min−1·mmHg−1, P = 0.09). With subsequent administration of ketorolac LVC decreased to 29.6 ± 2 ml·min−1·mmHg−1 ( P = 0.02; n = 9). While exercise continued, LVC returned to control values (33 ± 2 ml·min−1·mmHg−1) within 3 min, suggesting involvement of additional vasodilator mechanisms. In four additional subjects, LVC tended to decrease with l-NAME infusion alone ( P = 0.08) but did not demonstrate the transient recovery. Whole body and leg V̇o2 increased with exercise but were not altered by l-NAME or l-NAME + ketorolac. These data indicate a modest role for NOS- and COX-mediated vasodilation in the leg of exercising humans during prolonged steady-state exercise, which can be restored acutely. Furthermore, NOS and COX do not appear to influence muscle V̇o2 in untrained healthy young adults.

Contribution of BAT and skeletal muscle to thermogenesis induced by ephedrine in man

1985 ◽  
Vol 248 (5) ◽  
pp. E507-E515 ◽  
Author(s):  
A. Astrup ◽  
J. Bulow ◽  
J. Madsen ◽  
N. J. Christensen
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Local Temperature ◽  
Whole Body ◽  
Tissue Blood Flow ◽  
Muscle Oxygen ◽  
Brown Adipose ◽  
Muscle Oxygen Consumption

This investigation was performed to examine the role of brown adipose tissue (BAT) in thermogenesis induced by ephedrine in man. Light microscopy of biopsies from necropsy cases showed BAT to occur most frequently in the perirenal fat. Perirenal BAT thermogenesis was investigated in five lean men before and during stimulation with 1 mg ephedrine orally X kg body wt-1. Perirenal BAT thermogenesis was assessed by continuous measurements of local temperature and blood flow with the 133xenon clearance method. In the same study the effect of ephedrine on skeletal muscle oxygen consumption was estimated by measurements of leg blood flow and arteriovenous oxygen difference. The perirenal adipose tissue blood flow increased approximately twofold, whereas the local temperature increased approximately 0.1 degrees C on an average. Assuming that man possesses 700 g of BAT with a similar thermogenic capacity, this tissue contributed only 10 ml X min-1 to the 40 ml X min-1 increase in oxygen consumption in the subject whose perirenal BAT showed the most pronounced response to ephedrine. The leg oxygen consumption increased on an average 60% after ephedrine. By extrapolation of this value to whole body skeletal muscle, approximately 50% of the increase in oxygen consumption induced by ephedrine may take place in skeletal muscle. It is concluded that skeletal muscle is a tissue of importance with respect to the thermogenic effect of sympathomimetics in man, whereas the results do not support a major role for perirenal BAT.

Net uptakes of oestradiol-17β and progesterone across the portal-drained viscera and the liver of ewes

1994 ◽  
Vol 141 (2) ◽  
pp. 353-358 ◽  
Author(s):  
H C Freetly ◽  
C L Ferrell
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Portal Vein ◽  
Abdominal Aorta ◽  
Infusion Rate ◽  
Jugular Vein ◽  
Hepatic Uptake ◽  
Hepatic Tissue ◽  
Arterial Concentration ◽  
Net Uptake

Abstract The objective of this study was to determine whether circulating concentrations or prior exposure to oestradiol-17β (OE2) and progesterone affected their uptake by splanchnic tissues. Catheters were surgically placed in the portal vein, a branch of the hepatic vein, a mesenteric vein and the abdominal aorta of three multiparous ovariectomized Dorset ewes. Blood and plasma flow across the portal-drained viscera (PDV) and the liver, and net uptake of OE2 and O2 consumption in these same tissues were determined in ovariectomized ewes (control), during OE2 infusion into the jugular vein, 7 days after an OE2 implant had been given, and during OE2 infusion into the jugular vein 7 days after an OE2 implant. The above treatments were repeated for progesterone. Plasma flows across visceral organs were determined by marker dilution (para-aminohippuric acid), and OE2 and progesterone concentrations were determined by radioimmunoassay. During the infusion with OE2, OE2 arterial concentration (mean ± s.d.) was 346 ± 199 pg/ml, PDV net uptake was 9·7±5·6 μg OE2/h and hepatic net uptake was 15·5 ± 9·5 μg OE2/h. Hepatic uptake was 82% of the jugular OE2 infusion rate. Blood flow and oxygen consumption by hepatic tissue increased when ewes were exposed to an OE2 implant for 7 days. During the infusion with progesterone, progesterone arterial concentration (mean ± s.d.) was 8·8 ±3·4 ng/ml, PDV net uptake was 220 ± 118 μg progesterone/h and hepatic net uptake was 238 ± 52 μg progesterone/h. Hepatic net uptake was 23% of the progesterone jugular infusion rate. Journal of Endocrinology (1994) 141, 353–358

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