Glucose-induced thermogenesis in tetraplegic patients with low sympathoadrenal activity

1994 ◽  
Vol 266 (2) ◽  
pp. E161-E170
Author(s):  
A. K. Aksnes ◽  
T. Brundin ◽  
N. Hjeltnes ◽  
J. Wahren
Keyword(s):  
Healthy Subjects ◽  
Cervical Spinal Cord ◽  
Plasma Concentrations ◽  
Control Group ◽  
Arterial Blood ◽  
Sympathoadrenal Activity ◽  
Arterial Plasma ◽  
Arterial Blood Glucose ◽  
Blood Glucose Concentrations ◽  
Effect Of Glucose

The influence of the sympathoadrenal system on the thermic effect of glucose was examined by studying six tetraplegic patients with complete lesions of the cervical spinal cord. Indirect calorimetry and catheter techniques were employed, and measurements were made before and during 2 h after oral ingestion of 75 g of glucose. The results were compared with previous findings from an identical study in healthy subjects and with those from a control group of five tetraplegic patients receiving water instead of glucose. In response to glucose, energy expenditure rose from 69 +/- 5 to 79 +/- 5 and from 88 +/- 3 to 98 +/- 4 W, (not significant) in the patients and healthy subjects, respectively. In both patients and the healthy subjects the postprandial oxygen consumption increased exclusively in extrasplanchnic tissues. Splanchnic blood flow, which in normals increased 34 +/- 1%, did not change in the patients after glucose. Blood temperatures were unchanged in normals after glucose but rose by approximately 0.5 degrees C in the patients. The patients' arterial plasma concentrations of norepinephrine were low in the basal state and did not rise significantly after glucose. The arterial blood glucose concentrations after glucose were significantly higher in the patients than in the healthy subjects. Insulin levels rose to 105 +/- 20 mU/l in the patients and to 59 +/- 7 mU/l in the controls (P < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Nonhepatic response to portal glucose delivery in conscious dogs

2000 ◽  
Vol 279 (6) ◽  
pp. E1271-E1277 ◽  
Author(s):  
Mary Courtney Moore ◽  
Po-Shiuan Hsieh ◽  
Doss W. Neal ◽  
Alan D. Cherrington
Keyword(s):  
Glucose Uptake ◽  
Glucose Infusion ◽  
Glucose Load ◽  
Arterial Blood ◽  
Hepatic Glucose ◽  
The Difference ◽  
Arterial Plasma ◽  
Arterial Blood Glucose ◽  
Blood Glucose Concentrations ◽  
Hepatic Glucose Uptake

The glycemic and hormonal responses and net hepatic and nonhepatic glucose uptakes were quantified in conscious 42-h-fasted dogs during a 180-min infusion of glucose at 10 mg · kg−1 · min−1 via a peripheral (Pe10, n = 5) or the portal (Po10, n = 6) vein. Arterial plasma insulin concentrations were not different during the glucose infusion in Pe10 and Po10 (37 ± 6 and 43 ± 12 μU/ml, respectively), and glucagon concentrations declined similarly throughout the two studies. Arterial blood glucose concentrations during glucose infusion were not different between groups (125 ± 13 and 120 ± 6 mg/dl in Pe10 and Po10, respectively). Portal glucose delivery made the hepatic glucose load significantly greater (36 ± 3 vs. 46 ± 5 mg · kg−1 · min−1 in Pe10 vs. Po10, respectively, P < 0.05). Net hepatic glucose uptake (NHGU; 1.1 ± 0.4 vs. 3.1 ± 0.4 mg · kg−1 · min−1) and fractional extraction (0.03 ± 0.01 vs. 0.07 ± 0.01) were smaller ( P < 0.05) in Pe10 than in Po10. Nonhepatic (primarily muscle) glucose uptake was correspondingly increased in Pe10 compared with Po10 (8.9 ± 0.4 vs. 6.9 ± 0.4 mg · kg−1 · min−1, P < 0.05). Approximately one-half of the difference in NHGU between groups could be accounted for by the difference in hepatic glucose load, with the remainder attributable to the effect of the portal signal itself. Even in the absence of somatostatin and fixed hormone concentrations, the portal signal acts to alter partitioning of a glucose load among the tissues, stimulating NHGU and reducing peripheral glucose uptake.

scholarly journals The Effect of Bilateral Nephrectomy on Renalase and Catecholamines in Hemodialysis Patients

2021 ◽  
Vol 18 (12) ◽  
pp. 6282
Author(s):  
Magda Wiśniewska ◽  
Natalia Serwin ◽  
Violetta Dziedziejko ◽  
Małgorzata Marchelek-Myśliwiec ◽  
Barbara Dołęgowska ◽  
...  
Keyword(s):  
Healthy Subjects ◽  
Plasma Concentrations ◽  
Serum Levels ◽  
Hemodialysis Patients ◽  
Pressure Regulation ◽  
Serum Concentrations ◽  
Monoamine Oxidase Activity ◽  
Normal Kidney ◽  
Bilateral Nephrectomy ◽  
Arterial Blood

Background/Aims: Renalase is an enzyme with monoamine oxidase activity that metabolizes catecholamines; therefore, it has a significant influence on arterial blood pressure regulation and the development of cardiovascular diseases. Renalase is mainly produced in the kidneys. Nephrectomy and hemodialysis (HD) may alter the production and metabolism of renalase. The aim of this study was to examine the effect of bilateral nephrectomy on renalase levels in the serum and erythrocytes of hemodialysis patients. Methods: This study included 27 hemodialysis patients post-bilateral nephrectomy, 46 hemodialysis patients without nephrectomy but with chronic kidney disease and anuria and 30 healthy subjects with normal kidney function. Renalase levels in the serum and erythrocytes were measured using an ELISA kit. Results: Serum concentrations of renalase were significantly higher in post-bilateral nephrectomy patients when compared with those of control subjects (101.1 ± 65.5 vs. 19.6 ± 5.0; p < 0.01). Additionally, renalase concentrations, calculated per gram of hemoglobin, were significantly higher in patients after bilateral nephrectomy in comparison with those of healthy subjects (994.9 ± 345.5 vs. 697.6 ± 273.4, p = 0.015). There were no statistically significant differences in plasma concentrations of noradrenaline or adrenaline. In contrast, the concentration of dopamine was significantly lower in post-nephrectomy patients when compared with those of healthy subjects (116.8 ± 147.7 vs. 440.9 ± 343.2, p < 0.01). Conclusions: Increased serum levels of renalase in post-bilateral nephrectomy hemodialysis patients are likely related to production in extra-renal organs as a result of changes in the cardiovascular system and hypertension.

scholarly journals Effects of free fatty acids on hepatic glycogenolysis and gluconeogenesis in conscious dogs

2002 ◽  
Vol 282 (2) ◽  
pp. E402-E411 ◽  
Author(s):  
Chang An Chu ◽  
Stephanie M. Sherck ◽  
Kayano Igawa ◽  
Dana K. Sindelar ◽  
Doss W. Neal ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Blood Glucose ◽  
Blood Glucose Level ◽  
Free Fatty Acids ◽  
Glucose Level ◽  
Conscious Dogs ◽  
Arterial Blood ◽  
Plasma Ffa ◽  
Arterial Plasma ◽  
Arterial Blood Glucose

The aim of this study was to determine the effect of high levels of free fatty acids (FFA) and/or hyperglycemia on hepatic glycogenolysis and gluconeogenesis. Intralipid was infused peripherally in 18-h-fasted conscious dogs maintained on a pancreatic clamp in the presence (FFA + HG) or absence (FFA + EuG) of hyperglycemia. In the control studies, Intralipid was not infused, and euglycemia (EuG) or hyperglycemia (HG) was maintained. Insulin and glucagon were clamped at basal levels in all four groups. The arterial blood glucose level increased by 50% in the HG and FFA + HG groups. It did not change in the EuG and FFA + EuG groups. Arterial plasma FFA increased by ∼140% in the FFA + EuG and FFA + HG groups but did not change significantly either in the EuG or HG groups. Arterial glycerol levels increased by ∼150% in both groups. Overall (3-h) net hepatic glycogenolysis was 196 ± 26 mg/kg in the EuG group. It decreased by 96 ± 20, 82 ± 16, and 177 ± 22 mg/kg in the HG, FFA + EuG, and FFA + HG groups, respectively. Overall (3-h) hepatic gluconeogenic flux was 128 ± 22 mg/kg in the EuG group, but it was suppressed by 30 ± 9 mg/kg in response to hyperglycemia. It was increased by 59 ± 12 and 56 ± 10 mg/kg in the FFA + EuG and FFA + HG groups, respectively. In conclusion, an increase in plasma FFA and glycerol significantly inhibited hepatic glycogenolysis and markedly stimulated hepatic gluconeogenesis.

A negative arterial-portal venous glucose gradient decreases skeletal muscle glucose uptake

1998 ◽  
Vol 275 (1) ◽  
pp. E101-E111 ◽  
Author(s):  
Pietro Galassetti ◽  
Masakazu Shiota ◽  
Brad A. Zinker ◽  
David H. Wasserman ◽  
Alan D. Cherrington
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
External Iliac Artery ◽  
Baseline Period ◽  
Glucose Infusion ◽  
Whole Body ◽  
Arterial Blood ◽  
Arterial Plasma ◽  
Arterial Blood Glucose ◽  
Venous Glucose

The effect of a negative arterial-portal venous (a-pv) glucose gradient on skeletal muscle and whole body nonhepatic glucose uptake was studied in 12 42-h-fasted conscious dogs. Each study consisted of a 110-min equilibration period, a 30-min baseline period, and two 120-min hyperglycemic (2-fold basal) periods (either peripheral or intraportal glucose infusion). Somatostatin was infused along with insulin (3 × basal) and glucagon (basal). Catheters were inserted 17 days before studies in the external iliac artery and hepatic, portal and common iliac veins. Blood flow was measured in liver and hindlimb using Doppler flow probes. The arterial blood glucose, arterial plasma insulin, arterial plasma glucagon, and hindlimb glucose loads were similar during peripheral and intraportal glucose infusions. The a-pv glucose gradient (in mg/dl) was 5 ± 1 during peripheral and −18 ± 3 during intraportal glucose infusion. The net hindlimb glucose uptakes (in mg/min) were 5.0 ± 1.2, 20.4 ± 4.5, and 14.8 ± 3.2 during baseline, peripheral, and intraportal glucose infusion periods, respectively ( P < 0.01, peripheral vs. intraportal); the hindlimb glucose fractional extractions (in %) were 2.8 ± 0.4, 4.7 ± 0.8, and 3.9 ± 0.5 during baseline, peripheral, and intraportal glucose infusions, respectively ( P < 0.05, peripheral vs. intraportal). The net whole body nonhepatic glucose uptakes (in mg ⋅ kg−1⋅ min−1) were 1.6 ± 0.1, 7.9 ± 1.3, and 5.4 ± 1.1 during baseline, peripheral, and intraportal glucose infusion, respectively ( P < 0.05, peripheral vs. intraportal). In the liver, net glucose uptake was 70% greater during intraportal than during peripheral glucose infusion (5.8 ± 0.7 vs. 3.4 ± 0.4 mg ⋅ kg−1⋅ min−1). In conclusion, despite comparable glucose loads and insulin levels, hindlimb and whole body net nonhepatic glucose uptake decreased significantly during portal venous glucose infusion, suggesting that a negative a-pv glucose gradient leads to an inhibitory signal in nonhepatic tissues, among which skeletal muscle appears to be the most important.

Effect of human recombinant superoxide dismutase on canine myocardial infarction

1990 ◽  
Vol 258 (2) ◽  
pp. H369-H380 ◽  
Author(s):  
B. S. Patel ◽  
M. O. Jeroudi ◽  
P. G. O'Neill ◽  
R. Roberts ◽  
R. Bolli
Keyword(s):  
Superoxide Dismutase ◽  
Infarct Size ◽  
Low Dose ◽  
Coronary Occlusion ◽  
Plasma Concentrations ◽  
Control Group ◽  
High Dose ◽  
Collateral Flow ◽  
Tetrazolium Chloride ◽  
Arterial Blood

To determine whether human recombinant superoxide dismutase (h-SOD) produces sustained reduction of infarct size, anesthetized dogs underwent a 2-h coronary occlusion followed by either 48 or 4 h of reperfusion. In the 48-h study, dogs were randomized to three intravenous treatments: 1) “low-dose” h-SOD (2 mg/kg bolus 2 min before reperfusion followed by 4 mg/kg over 45 min), 2) “high-dose” h-SOD (8 mg/kg bolus 2 min before reperfusion followed by 8 mg/kg over 45 min), or 3) equivalent volumes of saline. In the 4-h study, dogs were randomized to high-dose h-SOD or saline. Occluded bed size was measured by postmortem perfusion and infarct size by triphenyl tetrazolium chloride staining and planimetry. Investigators performing the study and measuring infarct size were blinded to the treatment given. High plasma concentrations of h-SOD were present in the arterial blood of treated dogs in the early phase of reperfusion (greater than 60 and greater than 180 micrograms/ml in low- and high-dose groups, respectively). In both studies, control and treated groups were similar with respect to occluded bed size, collateral blood flow, and rate-pressure product during ischemia. In the 48-h study, infarct size, expressed as percent of occluded bed size, was 41.3 +/- 7.6% (mean +/- SE) in the control group, 37.1 +/- 7.2% in the low-dose h-SOD group, and 48.0 +/- 7.1% in the high-dose h-SOD group. In the 4-h study, infarct size was 30.6 +/- 4.9% in the control group and 31.5 +/- 9.6% in the high-dose h-SOD group. Analysis of the flow-infarct relationships confirmed that h-SOD did not reduce infarct size at any level of collateral flow in either the 48- or 4-h study. Recovery of regional myocardial function after reperfusion was also unaffected by h-SOD in both studies. Thus in this randomized blinded study, large doses of h-SOD given at the time of reperfusion failed to limit infarct size or enhance recovery of function, both early (4 h) and late (48 h) after reperfusion following a 2-h coronary occlusion.

Studies of experimental cervical spinal cord transection

1979 ◽  
Vol 50 (5) ◽  
pp. 629-632 ◽  
Author(s):  
Phillip A. Tibbs ◽  
Byron Young ◽  
Michael G. Ziegler ◽  
R. G. McAllister
Keyword(s):  
Spinal Cord ◽  
Cervical Spinal Cord ◽  
Plasma Concentrations ◽  
Spinal Cord Transection ◽  
Cervical Cord ◽  
Control Group ◽  
Content Type ◽  
Hemorrhagic Necrosis ◽  
Anesthetized Dogs ◽  
Experimental Group

✓ Plasma concentrations of norepinephrine (NE) were measured by a radioenzymatic assay technique before and serially after laminectomy at the C-6 level in 14 anesthetized dogs. In half the animals, no further procedures were carried out (control group); in the other dogs, cervical cord transection was performed in addition to laminectomy (experimental group). Mean plasma NE levels were similar in both groups after laminectomy and before cord interruption. In the control group, NE levels increased gradually for 2 hours after the procedure. In the group with cord transection, however, NE rose immediately after transection to 267% of the baseline value, then fell to 25% of the plasma NE level in the control group at 30 minutes, 29% at 60 minutes, and 15% at 120 minutes. Cervical spinal cord transection, therefore, results in an abrupt but short-lived increase in plasma NE concentrations. These changes in plasma NE levels may explain, at least in part, the hemodynamic alterations and the acute central hemorrhagic necrosis that occur after high spinal cord trauma.

Inclusion of low amounts of fructose with an intraportal glucose load increases net hepatic glucose uptake in the presence of relative insulin deficiency in dog

2005 ◽  
Vol 288 (6) ◽  
pp. E1160-E1167 ◽  
Author(s):  
Masakazu Shiota ◽  
Pietro Galassetti ◽  
Kayano Igawa ◽  
Doss W. Neal ◽  
Alan D. Cherrington
Keyword(s):  
Blood Glucose ◽  
Glucose Uptake ◽  
Control Period ◽  
Glucose Infusion ◽  
Control Group ◽  
Hepatic Glycogen ◽  
Arterial Blood ◽  
Hepatic Glucose ◽  
Arterial Blood Glucose ◽  
Hepatic Glucose Uptake

The effect of small amounts of fructose on net hepatic glucose uptake (NHGU) during hyperglycemia was examined in the presence of insulinopenia in conscious 42-h fasted dogs. During the study, somatostatin (0.8 μg·kg−1·min−1) was given along with basal insulin (1.8 pmol·kg−1·min−1) and glucagon (0.5 ng·kg−1·min−1). After a control period, glucose (36.1 μmol·kg−1·min−1) was continuously given intraportally for 4 h with (2.2 μmol·kg−1·min−1) or without fructose. In the fructose group, the sinusoidal blood fructose level (nmol/ml) rose from <16 to 176 ± 11. The infusion of glucose alone (the control group) elevated arterial blood glucose (μmol/ml) from 4.3 ± 0.3 to 11.2 ± 0.6 during the first 2 h after which it remained at 11.6 ± 0.8. In the presence of fructose, glucose infusion elevated arterial blood glucose (μmol/ml) from 4.3 ± 0.2 to 7.4 ± 0.6 during the first 1 h after which it decreased to 6.1 ± 0.4 by 180 min. With glucose infusion, net hepatic glucose balance (μmol·kg−1·min−1) switched from output (8.9 ± 1.7 and 13.3 ± 2.8) to uptake (12.2 ± 4.4 and 29.4 ± 6.7) in the control and fructose groups, respectively. Average NHGU (μmol·kg−1·min−1) and fractional glucose extraction (%) during last 3 h of the test period were higher in the fructose group (30.6 ± 3.3 and 14.5 ± 1.4) than in the control group (15.0 ± 4.4 and 5.9 ± 1.8). Glucose 6-phosphate and glycogen content (μmol glucose/g) in the liver and glucose incorporation into hepatic glycogen (μmol glucose/g) were higher in the fructose (218 ± 2, 283 ± 25, and 109 ± 26, respectively) than in the control group (80 ± 8, 220 ± 31, and 41 ± 5, respectively). In conclusion, small amounts of fructose can markedly reduce hyperglycemia during intraportal glucose infusion by increasing NHGU even when insulin secretion is compromised.

Low-dose flunarizine does not affect short-term fetal circulatory responses to acute asphyxia in sheep near term

1998 ◽  
Vol 10 (5) ◽  
pp. 405 ◽  
Author(s):  
Yves Garnier ◽  
Richard Berger ◽  
Doris Pfeiffer ◽  
Arne Jensen
Keyword(s):  
Low Dose ◽  
Plasma Concentrations ◽  
Neuronal Cell ◽  
Cardiovascular Responses ◽  
Control Group ◽  
Short Term ◽  
Fetal Sheep ◽  
Physiological Variables ◽  
Arterial Blood ◽  
Near Term

Asphyxia is one of the major causes of perinatal brain damage and neuronal cell loss, which may result in psychomotor deficits during later development. It has been shown previously that the immature brain can be protected from ischemic injury by flunarizine, a class IV calcium antagonist. However, cardiovascular side-effects of flunarizine, when applied at the dosages used in those studies, have been reported. Recently, the present authors were able to demonstrate that even by injecting flunarizine at a far lower dosage (1 mg kg) estimated bodyweight) neuronal cell damage, caused by occlusion of both carotid arteries for 30 min, can be reduced in fetal sheep near term. The aim of the present study was, therefore, to examine whether low-dose flunarizine affects fetal cardiovascular responses to acute asphyxia in sheep near term. Ten fetal sheep were chronically instrumented at a mean gestational age of 132 1 days (term is at 147 days). Fetuses from the study group received a bolus injection of flunarizine (1 mg kg–1 estimated fetal weight) 60 min before asphyxia, whereas the solvent was administered to the fetuses from the control group. Organ blood flows, physiological variables and plasma concentrations of catecholamines were measured before, during and after a single occlusion of uterine blood flow for 2 min (i.e. at 0, 1, 2, 3, 4, and 30 min). Before asphyxia, the distribution of combined ventricular output and physiological variables, as well as concentrations of catecholamines, in fetuses from the control group were in the normal range for chronically prepared fetal sheep near term. During acute asphyxia there was a redistribution of cardiac output towards the central organs accompanied by a pronounced bradycardia and a rapid increase in arterial blood pressure. After asphyxia circulatory centralization did not resolve quite as rapidly as it developed, but was almost completely recovered at 30 min after the insult. There were nearly no differences in the time course of physiological and cardiovascular variables measured before, during and after acute intrauterine asphyxia between the control and study groups. From the present study it was concluded that low-dose flunarizine does not affect short-term fetal circulatory responses to acute asphyxia in sheep near term.

scholarly journals Are Physiological Changes Experienced by Healthy Subjects during Acu-Tens Associated with Acupuncture Point Sensations?

2014 ◽  
Vol 32 (1) ◽  
pp. 28-36 ◽  
Author(s):  
David T W Yu ◽  
Alice Y M Jones
Keyword(s):  
Placebo Group ◽  
Healthy Subjects ◽  
Massachusetts General Hospital ◽  
Physiological Responses ◽  
Acupuncture Point ◽  
Control Group ◽  
Acupuncture Points ◽  
Physiological Changes ◽  
Arterial Blood ◽  
Experimental Group

Background Transcutaneous electrical nerve stimulation over acupuncture points (acu-TENS) has been reported to improve clinical outcomes. The objectives of the present study were to investigate whether acupuncture point sensations were experienced during acu-TENS, and whether such sensations were associated with any concomitant changes in autonomic nervous system activity. Methods This study adopted a single-blinded, randomised, controlled trial methodology. A total of 36 healthy subjects were randomly assigned to an experimental group (acu-TENS on right LI4 and LI11 points); control group (acu-TENS to bilateral kneecaps); or placebo group (sham acu-TENS on right LI4 and LI11 points). Heart rate (HR), mean arterial blood pressure (MAP), SD of the NN interval (SDNN) and low frequency to high frequency ratio (LF/HF) were measured before, during and after intervention. The Hong Kong Chinese version of the Massachusetts General Hospital Acupuncture Sensation Scale (C-MMASS) index was used for quantifying the acupuncture point stimulation sensations. Results The experimental group showed a significant increase in HR (mean (SD) 73.5 (6.3) to 75.9 (6.7) bpm, p=0.027), MAP (88.5 (4.5) to 91.0 (4.1) mm Hg, p=0.004), SDNN (143.36 (8.58) to 153.69 (7.64) ms, p=0.002) and LF/HF (1.26 (0.19) to 1.31 (0.21), p=0.037) during the intervention. The control group showed a significant increase in SDNN (140.21 (8.72) to 143.39 (9.47) ms, p=0.009) and LF/HF (1.21 (0.09) to 1.23 (0.12), p=0.033). There were no significant physiological changes in the placebo group. Overall C-MMASS indices for the experimental, control and placebo groups were 3.23 (0.3), 2.14 (0.6) and 0.29 (0.32), respectively. The between-group difference was statistically significant (F=139.24, df=2, p<0.05). However, correlation analysis did not support any association between sensation intensity and physiological responses in any groups (γ ranged from −0.36 to 0.25). Conclusions This study showed that ‘acupuncture point sensations’ were experienced during acu-TENS to LI4 and LI11, but such sensations were not associated with physiological responses induced during the stimulation.

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