Search PubMed⌕ Search

Biomedical subjects

B A Hansen

Publications and source records attributed to B A Hansen.

At least 73 records · Page 4Linked to original sources
PubMed1989

Neutral red changes arginine-induced glucagon and insulin response in the rat.

Rats were treated with neutral red (amino-dimethyl-amino-toluaminozine hydrochloride, NR) twice weekly, 5 ml/kg b.wt.-1 of a 2% solution, for five weeks in order to investigate damage to pancreatic A-cells. After 1-5 weeks of treatment plasma glucagon levels were increased to about two times control values. Plasma glucose was maintained at control values. Following arginine stimulation, 8 micrograms intravenously 100 g b.wt.-1 min.-1 for 30 min., plasma glucagon and insulin concentrations increased 10-fold in normal rats. After NR treatment for 1 and 2 weeks the arginine induced glucagon response was reduced to a two-fold increase, after 5 weeks NR treatment arginine again increased glucagon concentrations 10-fold. There was no change in the 10-fold increase of insulin concentrations from arginine infusion during the NR treatment. Immunohistochemical examination of pancreas demonstrated unchanged number and size of Langerhans' islets. The insulin immunoreactivity of the B-cells appeared constant 0-5 weeks during NR treatment, while glucagon immunoreactivity appeared to lower in the A-cells from animals treated for one or two weeks with NR. After three to five weeks of NR treatment, pancreatic glucagon immunoreactivity appeared restored. We conclude that NR leads to a release of glucagon from pancreatic A-cells, with subsequent hyperglucagonaemia, maintained during repeated administrations. Such repeated administrations lead to a transient "glucagon insufficiency" on top of the hyperglucagonaemia, consisting of restricted ability to further release of glucagon, presumably because of pancreatic A-cell glucagon depletion.

Animals↗
PubMed1988

Dexamethasone increases the capacity of urea synthesis time dependently and reduces the body weight of rats.

Rats of 230 g were treated with 0.1 mg of dexamethasone twice daily for 2 days (n = 5) and 14 days (n = 9). Controls received isotonic saline. During the first week of dexamethasone treatment the rats lost weight rapidly (up to 9 g/day). The weight loss diminished during the second week of treatment. The fasting blood insulin concentration increased sevenfold in the dexamethasone-treated rats. Fasting blood glucagon and glucose concentrations were not different from controls. In the dexamethasone-treated rats the fasting alpha-amino-N concentrations were lower: 4.0 +/- 0.3 mmol/l (mean +/- SEM) versus 6.8 +/- 0.3 mmol/l in controls. The capacity of Urea-N Synthesis, determined during alanine loading was: after 2 days of treatment 14.7 +/- 1.7 mumol/(min 100 g), after 14 days of treatment 7.9 +/- 0.8 mumol/(min 100 g), and in controls 7.5 +/- 1.0 mumol/(min 100 g) (mean +/- SEM). In conclusion, glucocorticoid treatment leads to a transient change in the liver function as to hepatic amino-N conversion, implying that more amino-N than normal is eliminated as urea-N after 2 days of treatment. This may contribute to the early, but not the late body weight loss.

Animals↗
PubMed1987

Time dependent stimulating effect of glucagon on the capacity of urea-N synthesis in rats.

The effect of glucagon on the capacity of urea-N synthesis was examined in 24 rats as a function of time. First, the conditions for saturation of urea synthesis under glucagon influence were studied by the kinetics of urea-N synthesis rate in relation to arterial blood alpha-amino-N concentration between 5 and 17 mmol/l in 21 nephrectomized rats given zinc-glucagon (20 micrograms s.c. per day) for 14 days. Alanine was infused so that steady state concentrations of total alpha-amino-N was attained in each rat. The urea-N synthesis rate was calculated as accumulation in total body water corrected for intestinal hydrolysis. The relationship suggested a barrier limited substrate inhibition kinetics, as earlier found in control rats, and data were examined accordingly by non-linear regression analysis. The estimated kinetic constants were: Vmax = 71 mumol/(min X 100 g body wt), Km = 5.4 mmol/l, Ki = 2.4 mmol/l, and the barrier = 4.4 mmol/l. Vmax was increased three times compared with controls. The capacity of urea-N synthesis, i.e. the zenith of the relation, was attained in the concentration interval 7.5 to 12.0 mmol/l, as in controls. The capacity of urea-N synthesis was determined during i.v. infusion of zinc-glucagon (0.15 microgram per min) and after 2, 8, and 14 days of daily s.c. injections of 20 micrograms zinc-glucagon. Rats given zinc-protamine solution were controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Hepatic regeneration following glucagon treatment.

Liver regeneration was studied as a function of time after suppression of the normal glucagon response. Rats were given a daily subcutaneous injection of 20 micrograms zincglucagon for 14 days, whereafter a 70% hepatectomy was performed. In the glucagon treated rats the rise in plasma glucagon concentration was diminished after hepatectomy. At intervals from 12 to 384 hours after hepatectomy, the gain in liver weight, the hepatic DNA content, and the antipyrine clearance were measured. All 3 variables were found to be significantly higher in animals with diminished glucagon response. The results indicate that prevention of the normal increase in glucagon concentration leads to signs of increased liver regeneration after 70% hepatectomy.

Animals↗
PubMed1986

Increased capacity of urea synthesis in streptozotocin diabetes in rats.

Diabetes was induced in Wistar rats by intravenous streptozotocin, 75 mg/kg. Four and 14 days after streptozotocin, fasting insulin decreased to about one-third, and fasting glucagon increased three-fold. The urea-N synthesis rate, stimulated by infusion of alanine, was measured at different amino acid concentrations 14 days after streptozotocin in 24 rats. The relationship was compatible with a barrier limited substrate inhibition kinetics. Data were examined accordingly by non-linear regression analysis. Among the estimated kinetic constants, only the 70% increase in Vmax was different from control values. In control rats the capacity of urea nitrogen synthesis, as measured within the amino acid concentration interval 7.3-11.6 mmol/l, was 10.2 +/- 1.1 mumol . (min 100 g BW)-1 (mean +/- SEM). The capacity was not different in 4 day diabetic rats, whereas it doubled in 14 day diabetic rats, 20.9 +/- 1.7 mumol (min 100 g BW)-1. The alanine elimination rate was 35% higher in the 14 day diabetic rats compared both to 4 day diabetic and control rats. The increase of urea synthesis is suggested to be due to enzyme induction by glucagon. The net nitrogen balance was negative at amino acid concentrations up to 25 mmol/l, indicating that the urea synthesis was increased at the expense of amino nitrogen.

Animals↗
PubMed1986

Fractures of the tibial shaft conservatively treated.

Strict conservative treatment of fractures of the tibial shaft using traction when there is difficulty in restoring length or axis has given excellent radiological results with very little residual deformity and no serious complications, but only at the cost of doubling the number of days in hospital compared with more recent operative series. For the longitudinal fractures the time to bearing full weight is twice that of the series treated by operation.

Casts, Surgical↗
PubMed1986

Starvation induced changes in quantitative measures of liver function in the rat.

Liver function was estimated quantitatively as the capacity of urea-N synthesis (CUNS), the galactose elimination capacity (GEC) and the antipyrine plasma clearance (APC) in rats following 24, 48, and 96 h of food deprivation. CUNS rose to a maximum following 24 h of starvation, then decreased to the control value at 48, 72, and 96 h (p = 0.02). GEC decreased following starvation, significant so at 48 h (p = 0.02). APC decreased at 48, and 72 h (p = 0.01), but rose to the control value at 96 h. It is concluded that a precise standardisation of starvation is important for interpretation of minor changes in CUNS, GEC, and APC.

Journal Article↗
PubMed1986

The capacity of urea-N synthesis as a quantitative measure of the liver mass in rats.

The capacity of urea-N synthesis (CUNS), the galactose elimination capacity (GEC) and the antipyrine clearance (APC) were measured in rats immediately after 30, 70 and 90% partial hepatectomy and after sham operation. CUNS was assessed during alanine infusion as urea accumulation in total body water, corrected for intestinal hydrolysis, and GEC was measured during constant galactose infusion in the same animals. APC was determined by the one-sample method in a separate group of animals, treated similarily. CUNS, GEC and APC were all correlated to the liver weight with correlation coefficients (r) above 0.8 and the correlation coefficients (r) between CUNS, GEC and APC were all above 0.7. It is concluded that CUNS is a quantitative measure of the functional liver mass in the rat.

Animals↗
PubMed1986

Insulin and glucose decreases the capacity of urea-N synthesis in the rat.

The relationship between insulin concentration (32-980 mU/l) and the capacity of urea-N synthesis (CUNS) was investigated with alanine as nitrogen source in 26 nephrectomized rats. The blood glucose concentration was kept constant by the 'glucose clamp' technique, and the endocrine pancreatic response was controlled by somatostatin. The CUNS was determined as the accumulation of urea corrected for intestinal hydrolysis at a constant amino acid concentration within the interval 7.3-11.6 mmol/l. At insulin concentration above 200 mU/l CUNS was decreased from 10 to 6 mumol (min X 100 g body wt)-1. At lower insulin concentrations the decrease was proportional. Hyperglycaemia 14.8 mmol/l decreased CUNS to 6.3 mumol (min X 100 g body wt)-1. The basal rate of urea-N synthesis was reduced from 3.8 to 1.9 mumol (min X 100 g body wt)-1 by insulin concentrations above 200 mU/l. The estimated alanine elimination (5.8 mumol(min X 100 g body wt)-1) was unchanged by insulin and reduced to 3.3 mumol(min X 100 g body wt)-1) by hyperglycaemia. Somatostatin infusion had no effect on CUNS or alanine elimination. It is suggested that the capacity of urea-N synthesis is subject to short term regulation independently by insulin and glucose.

Alanine↗
PubMed1985

A method for determination of the capacity of urea synthesis in the rat.

The relationship between total blood alpha-amino nitrogen concentration and urea synthesis rate was investigated with alanine as nitrogen source in 24 rats. Alanine was given as prime-continuous doses for 70 min so that constant amino acid concentration was attained between 5.5 and 34 mmol/l. Urea synthesis rate was assessed as accumulation in body water, corrected for intestinal hydrolysis. There was a positive correlation between nitrogen balance and alpha-amino nitrogen concentration. Urea synthesis rate in relation to amino acid concentration suggested barrier-limited substrate inhibition kinetics and data were examined accordingly by non-linear regression analysis. The estimated kinetic constants (mean +/- standard deviation) were: Vmax: 19.2 +/- 3.3 mumol (min X 100 g BW)-1, Km: 1.74 +/- 0.5 mmol/l, Ki: 6.84 +/- 1.9 mmol/l, and the barrier: 5.4 +/- 0.13 mmol/l. Because of the substrate inhibition, saturation cannot be attained, but the maximum synthesis rate, i.e. the capacity of urea nitrogen synthesis (CUNS), can be measured within 95% of the theoretical maximum in the concentration interval 7.3-11.6 mmol/l. CUNS was 9.16 +/- 0.81 mumol (min X 100 g BW)-1 (mean +/- standard deviation). Substrate-independent regulation of urea synthesis, e.g. by changes in liver mass or hormonal concentration, can be studied by this measure.

Alanine↗
PubMed1985

Increased intestinal hydrolysis of urea in patients with alcoholic cirrhosis.

Fourteen patients with biopsy-proven alcoholic liver cirrhosis in a clinically stable phase but with compromised liver function entered the study, together with 10 control persons. All had normal creatinine clearance, and none received antibiotics or hormones. They ingested a diet containing 1 g of protein/kg body weight daily during the study. The fractional intestinal loss of newly synthesized urea, determined by a 14C-urea tracer method, was increased from 0.17 +/- 0.08 in controls to 0.26 +/- 0.08 in cirrhotics (mean +/- SD, P less than 0.02). Urea nitrogen synthesis rate, determined as urinary excretion rate, corrected for accumulation in the total body water and for fractional intestinal loss, was the same in controls and cirrhotics (26.1 +/- 3.8 and 22.1 +/- 6.8 mmol/h, respectively). The patients with cirrhosis had a significantly greater nitrogen balance than the control group (12.5 +/- 7.0 mmol/h versus 7.0 +/- 5.9 mmol/h; P less than 0.05). Furthermore, there was a positive correlation between intestinal loss and blood urea nitrogen concentration (r = 0.68, P less than 0.01) in patients with cirrhosis but not in controls. The increased endogenous ammonia load of cirrhotics corresponds to an extra protein intake of 30-35 g/day. In patients with cirrhosis prophylactic treatment with, for example, lactulose is rational before reduction in dietary protein.

Adult↗
PubMed1984

Femoxetine clearance in patients with liver cirrhosis.

The pharmacokinetics of femoxetine (a 5-HT uptake inhibitor with antidepressive effect) was studied in 12 patients with liver cirrhosis and in 6 healthy controls after a single oral dose of femoxetine HC1. The average blood concentration of femoxetine, as assessed by the values of AUC (area under the plasma concentration/time curve), was significantly higher in the patients with liver cirrhosis than in the healthy controls in spite of dose reduction in the patients. The elimination half-life of femoxetine was within the normal limits in most of the patients. The oral clearance of femoxetine was considerably lower in patients, (0.65-4.02 1/hr/kg) than in the controls (8.13- greater than 50 1/hr/kg). It was not directly related to the metabolic function of the liver, measured as the galactose elimination capacity being 0.015-0.024 mmol/min./kg and 0.033-0.041 mmol/min./kg, respectively. When treating patients with reduced liver function, it is recommended to reduce the doses and to monitor closely the plasma levels.

Adult↗
PubMed1983

A case of malignant lymphoma and myasthenia gravis.

A 25-year-old man with myasthenia gravis and a non-Hodgkin lymphoma stage III B involving the thymus, is reported. The association myasthenia gravis and non-Hodgkin lymphoma has not been described previously. Treatment with chlormetin, vincristine, procarbazine, prednisone (MOPP) resulted in complete remission of both the myasthenic symptoms and the malignant lymphoma.

Adult↗