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Biomedical subjects

A Revhaug

Publications and source records attributed to A Revhaug.

At least 37 records · Page 2Linked to original sources
PubMed1997

Return of beta-adrenergic sensitivity in a patient with insulinoma after removal of the tumour.

Beta-adrenergic sensitivity and counterregulatory hormone and symptomatic responses to hypoglycaemia were studied in a 22-year-old man before and 3 and 34 weeks after removal of an insulinoma. The beta-adrenergic sensitivity was measured by the effect of an isoprenaline infusion on the heart rate, and the dose needed to increase the heart rate by 25 beats min(-1) (I25) calculated from regression lines. The glucose thresholds for the hormonal responses and symptoms were studied during a gradual fall in plasma glucose using a hypoglycaemic clamp technique. As compared with preoperative values, beta-adrenergic sensitivity was unchanged 3 weeks after surgery, but showed a marked improvement after 34 weeks, the I25 (in microg isoprenaline) being 0.96, 0.86, and 0.56, respectively. The hormone responses to hypoglycaemia were earlier, but with no improvement in symptom generation at 3 weeks. After 34 weeks, the thresholds for both hormone release and symptom generation occurred at a plasma glucose approximately 1 mmol l(-1) higher than before surgery. Thus, in our patient, there was a marked improvement in beta-adrenergic sensitivity, an earlier release of counterregulatory hormones, and an earlier recognition of hypoglycaemic symptoms after surgery. However, the restoration of these responses took more than 3 weeks.

Adrenergic beta-Agonists↗
PubMed1997

Adjuvant chemotherapy (5-fluorouracil and levamisole) in Dukes' B and C colorectal carcinoma. A cost-effectiveness analysis.

BACKGROUND: Adjuvant chemotherapy (5-fluorouracil, levamisole) is now standard practice in the treatment of Dukes' B and C coloretal carcinoma (CRC), and this has increased the financial burden on health care systems world-wide. PATIENTS AND METHODS: Between 1993 and 1996, 95 patients in northern Norway were included in a national randomised CRC study, and assigned to surgery plus adjuvant chemotherapy or surgery alone. In April 1996, 94 of the patients were evaluable and 82 were still alive. The total treatment costs (hospital stay, surgery, chemotherapy, administrative and travelling costs) were calculated. A questionnaire was mailed to all survivors for assessment of the quality of their lives (QoL) (EuroQol questionnaire, a simple QoL-scale, global QoL-measure of the EORTC QLQ-C30), and 62 of them (76%) responded. RESULTS: Adjuvant chemotherapy in Dukes' B and C CRC raised the total treatment costs by 3,369 pounds. The median QoL was 0.83 (0-1 scale) in both arms. Employing a 5% discount rate and an improved survival of adjuvant therapy ranging from 5% to 15%, we calculated the cost of one gained quality-adjusted life-year (QALY) to be between 4,800 pounds and 16,800 pounds. CONCLUSION: Using a cut-off point level of 20,000 pounds per QALY, adjuvant chemotherapy in CRC appears to be cost-effective only when the improvement in 5-year survival is > or = 5%. Adjuvant chemotherapy does not affect short-term QoL.

Adult↗
PubMed1997

Both growth hormone and exogenous glutamine increase gastrointestinal glutamine uptake in trauma.

OBJECTIVE: The authors studied the effect of exogenous glutamine (GLN), with and without growth hormone (GH), pretreatment, on gastrointestinal, hepatic, femoral, and renal GLN fluxes. SUMMARY BACKGROUND DATA: Growth hormone treatment increases gastrointestinal uptake of GLN despite a reduced skeletal muscle and whole body release. METHODS: Piglets were randomized to a GH + GLN group (n = 8), a GLN group (n = 8), a GH group (n = 8), and a control group (CON; n = 8). Genotropin (Pharmacia, Stockholm, Sweden; 24 international units; correspondingly saline in the GLN and the CON group) was given daily 3 days before and at the onset of trauma (surgery). Organ fluxes and whole body release of GLN were determined 1 and 5 hours after surgery. An infusion of GLN 36 micrograms/kg per minute was started after the first measurement in the GH + GLN and the GLN groups. RESULTS: Both GH treatment and exogenous GLN increased gastrointestinal GLN uptake (p = 0.001 and p = 0.02, respectively). Growth hormone treatment reduced hepatic GLN uptake (p = 0.001). Hepatic GLN uptake was lower in the GH + GLN group versus the GH group (p = 0.02), but not in the GLN group versus the CON group (p = 0.98). Growth hormone treatment reduced femoral and whole-body GLN release (p = 0.0001 and p = 0.02, respectively). Renal GLN uptake was higher in the two GH-treated groups (p = 0.003). CONCLUSION: Both exogenous GLN and GH increased gastrointestinal GLN uptake, and the combination was additive. In contrast to exogenous GLN, GH reduced hepatic uptake and consequently facilitated the increased gastrointestinal GLN uptake that occurred despite reduced femoral and whole-body release.

Animals↗
PubMed1997

The influence of growth hormone on tumour necrosis factor and neutrophil leukocyte function in sepsis.

The aim of this study was to assess the influence of growth hormone (GH) in sepsis on the immune system represented by the circulating TNF-levels and the neutrophil leukocytes phagocytic capacity and respiratory burst, 22 piglets were randomized to 3 groups; pretreatment with GH (16 i.u.) before sepsis (n = 8), non-treated septic controls (n = 8), and non-septic controls (n = 6). Sepsis was induced by a standardized infusion of live E. coli. TNF was measured by a cytotoxic bioassay, while neutrophil function tests were carried out by flowcytometric assays. In brief, phagocytosis was evaluated by the neutrophils' ability to ingest FITC-labelled (fluorescein isothiocyanate) E. coli and intracellular release of oxygen metabolites was detected by the oxidation of 2',7'-dichlorofluorescin (DCFH) to the fluorescent 2',7'-dichlorofluorescein (DCF). Our data show a suppression of phagocytosis in the GH-treated group before sepsis; however, when challenged with Gram-negative bacteria, the phagocytic capacity was similar to that of the non-treated animals. The serum levels of TNF in the non-treated septic control group were twice the levels of those in the GH-treated group, 65.7 pg/ml (septic controls) vs 32.8 pg/ml (GH). Pretreatment with a single dose of GH few hours prior to sepsis does not seem to entail any further imbalance of the neutrophil function in sepsis. Lowering of the circulating TNF-levels is a presumptive favourable effect of GH in sepsis.

Animals↗
PubMed1997

Growth hormone increases and IGF-1 reduces the response to Escherichia coli infusion in injured pigs.

OBJECTIVE: To investigate if growth hormone (GH) or its main mediator insulin-like growth factor-1 (IGF-1) alters the response to infusion of live Escherichia coli in injured pigs. DESIGN: Controlled experiment. SETTING: University laboratory, Norway. SUBJECTS: 30 piglets. INTERVENTIONS: The response to infusion of Escherichia coli was compared after a bolus of GH 16 IU (n = 8) or a continuous infusion of IGF-1 1.3 mg/hour (n = 8) in injured piglets. A group with trauma (surgery) and Escherichia coli infusion (n = 8) and a group with trauma only (n = 6) served as controls. MAIN OUTCOME MEASURES: Systemic and regional haemodynamics, oxygen consumption, and acid-base regulation; and circulating concentrations of catecholamines, free fatty acids (FFA), glucose, and lactate Results: After infusion of Escherichia coli, cardiac output was lower and heart rate was higher in the GH than in the IGF-1-treated group. Aortic pH was lower in the GH group compared with the septic controls, whereas aortic pH was higher in the IGF-1 group compared with the septic controls. Portal vein pH was lower in the GH group than in the other three groups. Free fatty acids and lactate concentrations were higher in the GH group than in the other three groups. Glucose concentrations were lower in the IGF-1 group than in the other three groups. Renal artery flow was higher in the IGF-1 than in the GH group and the septic controls. Circulating concentrations of dopamine was higher in the IGF-1 group than in the other three groups, whereas that of noradrenaline was higher in the GH group than in the IGF-1 group. (For all differences stated, p < 0.05). CONCLUSIONS: Acute treatment with GH increased the circulatory and metabolic response to Escherichia coli infusion, in contrast to treatment with IGF-1, which reduced the response

Analysis of Variance↗
PubMed1996

Growth hormone pre-treatment combined with exogenous glutamine induced a postoperative shift from glucose to glutamine consumption in the gastrointestinal tract.

The aim of this study was to assess whether the protein sparing effects associated with administration of growth hormone (GH) and glutamine in the early post traumatic period deprive the gastrointestinal tract of substrates. Sixteen piglets were randomized to receive GH treatment (n = 8) for 3 days prior to surgery whilst a control group (n = 8) received no growth hormone. Organ fluxes of glucose, lactate, pyruvate, alanine and glutamine were measured at 1 and 5 h after surgery. An infusion of glutamine (36 microg/kg/min) was started after the first measurement in both groups. In the GH group (5 h after surgery), hindleg release of glutamine and alanine was found to be lower than in the control group, whilst intestinal glutamine uptake was higher and that of alanine was lower. Hepatic alanine uptake was reduced whilst hepatic glutamine exchange switched from uptake to release. Intestinal glucose consumption was lower in the GH group (P < 0.05). It is concluded that GH pre-treatment in combination with exogenous glutamine administration induced a shift in gastrointestinal fuel selection which was associated with reduced glucose consumption and increased glutamine consumption. The effect of GH in inducing hepatic release of glutamine compensated for its effect on muscle which results in reduced peripheral glutamine release.

Journal Article↗
PubMed1996

Acute growth hormone injection reduced gastrointestinal and increased hepatic oleic acid oxidation in swine.

Gastrointestinal, hepatic, and hindleg oxidation of 3H-labelled oleic acid and 14C-labelled glucose based on arterial-venous differences in 3H2O and 14CO2 were studied before and after an intravenous injection of 24 IU of growth hormone in 10 piglets. Hepatic oleic acid oxidation increased transiently while gastrointestinal oleic acid oxidation decreased correspondingly, maintaining a constant splanchnic oleic acid oxidation. Administration of a growth hormone led to a transient, parallel decrease in both hepatic and gastrointestinal glucose oxidation. We conclude that, in contrast to the growth hormone effect on splanchnic glucose oxidation, growth hormone effect on splanchnic fat oxidation appears to be organ specific.

Animals↗
PubMed1996

Growth hormone impaired compensation of hemorrhagic shock after trauma and sepsis in swine.

OBJECTIVE: To study hemodynamic effects of growth hormone (GH) and its main mediator, insulin-like growth factor-1, in a model of critical illness. DESIGN: Randomized experiment in traumatized and septic piglets. MATERIALS AND METHODS: Hemodynamics and blood gases before and sustained volume loss during a controlled, fatal hemorrhage were recorded in a GH treated group (n = 8), an insulin-like growth factor-1 treated group (n = 8), a control group with trauma and sepsis (n = 8), and a control group with trauma only (n = 6). MEASUREMENTS AND MAIN RESULTS: Sustained volume loss before cardiac arrest was lower in the GH group. The GH group was characterized by metabolic acidosis. During the hemorrhage, visceral blood flow (portal and renal) as a fraction of cardiac output (fractional flow) was lower and peripheral fractional flow higher in the GH group. Fractional renal artery flow was higher in the insulin-like growth factor-1 group (p < 0.05 for the comparisons stated). CONCLUSION: GH promoted metabolic acidosis in traumatized sepsis and impaired compensation of a subsequent hemorrhage.

Acidosis↗
PubMed1996

Effects of endothelin-1 on hepatic blood flow.

Endothelin-1 belongs to a family of potent vasoconstrictors, recently isolated from endothelial cells. Endothelin-1 has a variety of hepatic effects and hepatic clearance from the circulation is important. Elevated plasma concentrations of Endothelin-1 are found after orthotopic liver transplantation and in cirrhosis with ascites. This study in piglets on hepatic bloodflow was designed to compare differences in effects between central venous and intraportal injection of endothelin-1, and to evaluate effects of repeated injections. Central venous injection of endothelin-1 caused a larger reduction in portal vein flow, while intraportal injection caused a larger increase in portal vein pressure. Repeated injections resulted in a reduction in portal vein flow and an increase in portal vein vascular resistance.

Animals↗
PubMed1995

Experimental study to show that growth hormone treatment before trauma increases glutamine uptake in the intestinal tract.

This study examined whether growth hormone treatment deprived the intestinal tract of glutamine after trauma. Piglets were treated with growth hormone 24 units daily 3 days before and at the start of the trauma (GH-3, n = 8) or at the start of the trauma only (GH-1, n = 8). Eight piglets acted as non-treated controls. The trauma consisted of a standardized abdominal surgical procedure. Primed constant infusions of U-14C-glutamine were given. Intestinal, hepatic, renal and hindleg glutamine fluxes were measured. Growth hormone treatment increased mean(s.e.m.) net intestinal glutamine uptake: GH-3, 39.7(9.4) and 48.7(12.7) mumol/min; GH-1, 33.2(5.5) and 25.7(12.3) mumol/min; controls, 19.5(10.3) and 2.0(15.3) mumol/min at 1 h and 5 h after trauma, respectively, (P = 0.02). The treatment increased glutamine oxidation (P = 0.025), and decreased hindleg glutamine net (P = 0.0052) and absolute release (P = 0.0063), glutamine rate of appearance (P = 0.01), and percentage of glucose coming from glutamine (P = 0.05). Growth hormone treatment before trauma increased intestinal glutamine uptake.

Abdomen↗
PubMed1995

Perioperative use of total parenteral nutrition. Variations in guidelines and practice in three Norwegian hospitals.

In a cross-sectional, retrospective study of 604 cases, variations among three Norwegian hospitals in use of perioperative parenteral nutrition (TPN) after gastrointestinal surgery was determined. Postoperative TPN rates were 25%, 34% (p = .05) and 56% (p < .0001), respectively. However, a substantial part of the variation was explained by differences in patient characteristics.

Adolescent↗
PubMed1995

Influence of intra-osseous infusion of a small volume of hyperosmotic fluid on beta-adrenergic function in circulating lymphocytes from bled pigs.

The regulation of beta-adrenergic function in circulating mononuclear leukocytes was evaluated during an episode of haemorrhagic shock treated by intra-osseous infusion of a small volume of hyperosmotic fluid. Two groups of piglets (n = 14) were anaesthetized with ketamine and bled to a mean arterial pressure of 40 mmHg. After 45 min the animals were randomized to receive 100 ml of either hyperosmotic (2.4 mol l-1) or iso-osmotic (0.29 mol l-1) fluid (equal volumes of glucose/sodium chloride) into the tibial bone marrow. Observations of haemodynamic variables and levels of plasma catecholamines and cAMP of circulating mononuclear leukocytes were carried out for 70 min. Infusion of hyperosmotic fluid enhanced the circulatory performance and attenuated the plasma catecholamine release significantly (p < 0.05) compared to the corresponding values in the animals that had iso-osmotic fluid infusion. Measurements of unstimulated and isoprenaline-stimulated cAMP levels in mononuclear lymphocytes indicated that the high plasma catecholamine levels in the iso-osmotic treatment group induced a desensitization of the beta-adrenoceptors 70 min after initiation of the shock. This effect was not seen in animals that had undergone hyperosmotic infusion.

Animals↗
PubMed1995

Fatal myocardial depression and circulatory collapse associated with complement activation induced by plasma infusion in severe porcine sepsis.

We have previously reported that fresh frozen plasma (FFP) may induce a rapid irreversible shock when repeatedly infused in pigs challenged with Gram-negative sepsis. The aims of the present study were to elucidate the cardiovascular nature of the shock and determine the aetiologic role of tumour necrosis factor (TNF), complement activation and halothane anaesthesia. Three groups of anaesthetized piglets were inoculated with a lethal dose of live E. coli bacteria. Groups I (n = 8) and III (n = 8) were anaesthetized with halothane and group II (n = 8) with ketamine. Animals in groups I and II received repeated infusions of FFP, whereas animals in group III received repeated infusions of 7% albumin. Six animals in group I and four animals in group II died during the first plasma infusion. Survival time was significantly longer in group II (P = 0.04) compared to group I. No animals in group III died during the albumin infusions, and no adverse effects were observed during the infusions. In group I the plasma induced shock was characterized by abruptly falling mean arterial pressure, cardiac index, systemic vascular resistance index and left ventricular contractility. Concomitant increases were recorded in left ventricular filling pressure and central venous pressure. Group II demonstrated a similar, but delayed response. Plasma infusion was associated with a significant increase in terminal complement complex (TCC) (P < 0.03 in group I, P < 0.05 in group II) and depletion of serum ionized calcium. We conclude that FFP may induce fatal myocardial depression and circulatory collapse in severe sepsis. Complement activation may be of aetiologic importance.

Albumins↗
PubMed1995

Effect of haemorrhagic shock and intraosseous resuscitation on plasma and urine catecholamine concentrations and urinary clearance in pigs.

OBJECTIVE: To evaluate the plasma and urinary catecholamine concentrations after episodes of haemorrhagic shock treated by intraosseous infusion of a small volume of hyperosmotic fluid, followed by whole blood, in a standard porcine model. DESIGN: Randomised open study. SETTING: University hospital, Norway. MATERIAL: 18 piglets. INTERVENTIONS: All animals were bled to an arterial systolic pressure of 60 mm Hg. After 30 minutes 100 ml hyperosmotic (2.4 mol/l) fluid (glucose/sodium chloride) was given either intraosseously (n = 6) or intravenously (n = 6). Ninety minutes later the animals were again bled to a systolic pressure of 60 mm Hg, and after 30 minutes an autologous whole blood transfusion was given by either intraosseous or intravenous infusion. Six animals acted as untreated controls. MAIN OUTCOME MEASURES: Changes in haemodynamic variables and plasma and urinary catecholamine concentrations. RESULTS: Two pigs in the control group died. The hyperosmotic infusion improved the circulatory performance significantly (p < 0.05). Thirty minutes after both bleeds the plasma catecholamine concentrations were increased by 10-15 times, but returned to the reference range in all groups 90 minutes after the hyperosmotic infusion. Two hours after the whole blood infusion the catecholamine concentrations of the treated animals were at baseline values, significantly lower than those of the controls. The corresponding urinary catecholamine concentrations of the controls were significantly increased. There were no differences between the two treatment groups. CONCLUSION: The catecholamine measurements indicate that there may possibly be protective renal excretion of excess shock-induced plasma catecholamines after acute haemorrhage.

Animals↗