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Biomedical subjects

H Abrahamsson

Publications and source records attributed to H Abrahamsson.

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

Zinc absorption and achlorhydria.

Zinc absorption from 40 mumol of zinc in a water solution and from a test meal containing 22 mumol of zinc was studied in 8 patients with achlorhydria (no basal acid secretion and no secretion after pentagastrin stimulation). The test dose and the meal was labelled with 0.1 MBq of 65Zn and absorption was determined from measurement of the whole-body retention of the isotope. Zinc absorption was 68 +/- 16 per cent (mean +/- s.d.) from the water solution and 33 +/- 10 per cent from the test meal. The results did not differ from absorption in control subjects and indicate that achlorhydria per se does not affect zinc absorption.

Achlorhydria↗
PubMed1988

Measurements of membrane potential, transmembrane 45Ca fluxes, cytoplasmic free Ca2+ concentration and insulin release by transplantable rat insulinoma cells maintained in tissue culture.

Regulation of insulin release, membrane potential, transmembrane 45Ca fluxes and cytoplasmic free Ca2+ concentration, [Ca2+]i, was examined using suspensions of transplantable NEDH rat insulinoma cells previously cultured for 2-3 days to eliminate necrotic tumour cells and counter prior hypoglycaemia. Insulinoma cells displayed a resting [Ca2+]i of 94 +/- 8 nM (n = 17) and released 104 +/- 15 ng insulin 10(-6) cells (n = 7) during 60 min incubations with uptake of 2.7 +/- 0.2 nmol 45Ca 10(-6) cells (n = 7). High concentrations of glucose did not affect membrane potential, transmembrane 45Ca fluxes, [Ca2+]i or insulin release by insulinoma cells. K+ at 25 mM depolarised the plasma membrane, induced a small increase in 45Ca efflux and increased [Ca2+]i by 65%. This modest action was not associated with demonstrable effects on 45Ca uptake and insulin release. The effect of 25 mMK+ on [Ca2+]i was counteracted by D-600, but this blocker of voltage-activated Ca2+ channels and verapamil lacked effects on transmembrane 45Ca fluxes and insulin release. The Ca2+-calmodulin antagonist, trifluoroperazine, was also without effect on 45Ca fluxes and insulin release. Ca2+ ionophore ionomycin increased [Ca2+]i, whereas A23187 and X537A did not affect transmembrane 45Ca fluxes. Moreover, insulin release was independent of extracellular Ca2+ over the range 0-20.4 mM despite marked affects on transmembrane 45Ca fluxes and a greater than 4-fold change of [Ca2+]i. Dibutyryl cyclic AMP increased insulin release by 55% without affecting transmembrane 45Ca fluxes or [Ca2+]i. The phosphodiesterase inhibitor, theophylline, also enhanced insulin release by 10-36% with no change of 45Ca uptake. The effectiveness of theophylline was independent of extracellular Ca2+ over the range 0-10.2 mM. These results indicate that inappropriate Ca2+ regulation is a key pathogenic feature underlying the inappropriate insulin secretion of rat insulinoma cells.

Adenoma, Islet Cell↗
PubMed1988

Gastrointestinal and colonic segmental transit time evaluated by a single abdominal x-ray in healthy subjects and constipated patients.

Gastrointestinal transit time (GITT) and segmental colonic transit times were studied in 56 healthy subjects by repeated daily ingestion of 10 radiopaque markers followed by abdominal x-ray. A seven-day procedure including marker intake for 6 days and a single radiograph on day 7 was found to be a simple method to differentiate between rapid, normal and prolonged transit. Addition of 20 distinguishable markers on day 6 helped to describe transit profiles. Healthy women had longer GITT than men (median 2.4 and 1.9 days, respectively) measured as mean 50% excretion time for the ingested doses of markers. For comparisons with patients percentiles for transit were calculated. In constipated patients the 7-day method demonstrated prolonged GITT as well as transit dysfunction in separate colonic segments. The method seems convenient for clinical use in diagnostic as well as therapeutic studies of colonic transit.

Adult↗
PubMed1987

Gastrointestinal motility in patients with the irritable bowel syndrome.

Patients with the irritable bowel syndrome (IBS) often have symptoms from both proximal and distal parts of the gut. Motility disturbances have been reported to occur from the esophagus to the distal colon in IBS patients. The patients often have a decreased lower esophageal sphincter pressure and various abnormalities of esophageal peristalsis. Mean transit time in the small intestine after a meal is short in patients with diarrhoea, and long in patients with constipation and pain compared with normals. IBS patients also show abnormalities of the interdigestive MMC, particularly when exposed to stressful stimuli. Previous studies of the colonic oscillating control potential suggested an increased prevalence of 3/min. slow waves in IBS patients compared with normals, but later studies could not confirm this. Long time measurements with multiple electrodes along the colon show a high prevalence of short-lasting segmental contractions in constipated patients, while both short and long-lasting contractions are decreased in painless diarrhoea. Rectal recordings in IBS patients have shown an increased contractile response up to 3 hrs after a meal. --The disturbed gut motility in IBS patients seems to be due no neural influences rather than strictly myogenic factors.

Colon↗
PubMed1986

Beta adrenergic influence on oesophageal peristalsis in man.

The effects of the beta-1 adrenergic agonist prenalterol and the beta-2 adrenergic agonist terbutaline on oesophageal peristalsis were studied in nine healthy volunteers with pressures recorded in the proximal, middle, and distal oesophagus. Two doses of the agonists were given after pretreatment with placebo, propranolol, or metoprolol in a double blind randomised fashion. Terbutaline 0.25 +/- 0.25 mg iv decreased peristaltic pressure in middle oesophagus from 8.1 +/- 1.1 to 5.1 +/- 0.8 kPa (p less than 0.01) and in the distal oesophagus from 9.5 +/- 1.0 to 4.7 +/- 0.6 kPa (p less than 0.001). Peristaltic velocity was decreased in the distal oesophagus after terbutaline from 3.3 +/- 0.2 cm/sec to 2.9 +/- 0.2 cm/sec (p less than 0.05). Prenalterol 1 mg iv was followed by a decrease of peristaltic pressure in the middle oesophagus from 10.2 +/- 1.3 to 7.7 +/- 1.1 kPa (p less than 0.01) and a decrease of peristaltic velocity in upper oesophagus from 3.6 +/- 0.2 to 3.3 +/- 0.1 cm/sec (p less than 0.05) while no significant changes were seen in the distal oesophagus. Pretreatment with the beta-1 blocker metoprolol 15 mg iv blocked the effects of prenalterol 1 mg iv but not the effects of terbutaline. Propranolol 10 mg iv blocked the effects of terbutaline on peristaltic pressure. After metoprolol infusion mean distal peristaltic amplitude was 11.9 +/- 0.8 kPa compared with 8.5 +/- 1.2 kPa after placebo (p less than 0.01). It is concluded that both beta-1 and beta-2 adrenoceptor stimulation significantly decrease oesophageal peristaltic pressure in man. The body of the oesophagus seems to be under beta adrenergic inhibitory influence under physiological conditions.

Adrenergic beta-Agonists↗
PubMed1986

Intestinal fluid and electrolyte transport in man during reduced circulating blood volume.

The effect on intestinal net transport of fluid and electrolytes of a reduced circulating blood volume was studied in the human jejunum with the triple lumen perfusion technique. The blood volume was reduced by changing the lower extremities from an elevated to a dependent position combined with a venous stasis. The tilting manoeuvre, probably resembling a bleeding of about 600-800 ml, significantly increased net absorption of fluid, sodium and chloride while glucose transport was unaffected. Concomitantly the blood flow decreased and vascular resistance increased in the forearm vascular bed. The results are consistent with the hypothesis that activity in the sympathetic nervous system initiated from unloading of the cardiopulmonary volume receptors enhances intestinal absorption of fluid and electrolytes. The results also indicate that the human intestines are an important target organ in the compensatory mechanisms activated during hypovolaemia due to - for example, haemorrhage.

Adult↗
PubMed1986

Non-adrenergic non-cholinergic nervous control of gastrointestinal motility patterns.

Non-adrenergic non-cholinergic neurons seem to play an important role in regulation of movements in all parts of the gut. Inhibitory non-adrenergic non-cholinergic neurons mediate a number of descending and ascending reflex effects of physiological and pathophysiological relevance. However, our knowledge in this field is still limited. Development of specific blockers for the non-adrenergic non-cholinergic transmitter substances would help to increase our understanding of gastrointestinal motor functions in health and disease.

Animals↗
PubMed1985

Direct measurements of increased free cytoplasmic Ca2+ in mouse pancreatic beta-cells following stimulation by hypoglycemic sulfonylureas.

The effects of the hypoglycemic sulfonylureas tolbutamide and glibenclamide on free cytoplasmic Ca2+, [Ca2+]i, were compared with that of a depolarizing concentration of K+ in dispersed and cultured pancreatic beta-cells from ob/ob mice. [Ca2+]i was measured with the fluorescent Ca2+-indicator quin2. The basal level corresponded to 150 nM and increased to 600 nM after exposure to 30.9 mM K+. The corresponding levels after stimulation with 1 microM glibenclamide and 100 microM tolbutamide were 390 and 270 nM respectively. K+ depolarization increased [Ca2+]i more rapidly than either of the sulfonylureas. It is suggested that the increased [Ca2+]i obtained after stimulation by sulfonylureas is due to depolarization of the beta-cells with subsequent entry of Ca2+ through voltage-dependent channels.

Aminoquinolines↗
PubMed1985

Effects of beta-adrenoceptor stimulation on rectosigmoid motility in man.

Effects of selective beta-adrenoceptor agonists on rectosigmoid motility during prolonged rectal distension were studied in 12 healthy volunteers in a double-blind, randomized fashion. Continuous distension was performed with a balloon in the proximal part of the rectum. Pressure was recorded by this balloon and by a catheter in the sigmoid. Contractile activity was quantified for three consecutive periods of 25 min. On separate days prenalterol (beta-1 agonist), terbutaline (beta-2 agonist), and placebo, respectively, were administered intravenously preceded by a control period. Terbutaline, 0.5 mg intravenously, was followed by a significant decrease of sigmoid motility from 4.3 +/- 1.5 (SEM) kPa X min to 2.9 +/- 1.0 kPa X min (P less than 0.01) and of rectal motility from 4.3 +/- 1.3 to 2.4 +/- 0.7 kPa X min (P less than 0.05). After placebo a slight, but not significant, increase of contractile activity was seen compared to the initial control period. The effects of prenalterol, 1.0 and 4.0 mg intravenously, on motility did not differ from that of placebo infusion. Both drugs caused a dose-dependent increase of systolic blood pressure and of heart rate. The study shows that beta-2-adrenoceptor stimulation decreases rectosigmoid colonic pressure in man, while effects of beta-1 stimulation on motility index do not differ from that of placebo.

Adrenergic beta-Agonists↗
PubMed1985

Isolation of a purified mitochondrial fraction from viable clonal insulin-producing cells (RINm5F) by Percoll density gradient centrifugation.

A Percoll density gradient was employed for selecting large numbers of viable insulin-producing RINm5F cells. Homogenates of these cells were then subjected to gradient centrifugation and two clearly visible bands were obtained. The light fraction was essentially composed of mitochondria banded at a density of about 1.06 g/ml. The heavier fraction banded at 1.09 to 1.10 g/ml and contained lysosomes and a small number of secretory granules. The distribution of Percoll particles was restricted to the extracellular space and there was no adsorption to any membrane structures. The distribution pattern of marker enzymes for the mitochondria and lysosomes was similar to that of normal pancreatic beta-cells. With the use of a Percoll density gradient it was thus possible to isolate a purified mitochondrial fraction from viable RINm5F cells.

Animals↗
PubMed1985

Cyclic AMP potentiates glucose-induced insulin release from mouse pancreatic islets without increasing cytosolic free Ca2+.

The effects of various stimulants of insulin release on cytosolic free Ca2+, [Ca2+]i, in dispersed and cultured pancreatic beta-cells from ob/ob-mice were studied using the indicator quin-2, which in itself has only slight effects on the glucose-induced insulin release and the metabolism of the sugar. The resting [Ca2+]i was 158 +/- 7 nM. After increasing glucose to 20 mM there was a lag-period of 1-2 min before [Ca2+]i gradually rose, reaching a new plateau 60% higher after 5-6 min. Increasing intracellular cyclic AMP by adding forskolin did not further increase [Ca2+]i; on the contrary there was a slight temporary reduction despite a doubling of insulin secretion. The maintenance of the beta-cell function was evident from a marked increase of cytosolic [Ca2+]i after depolarization evoked by high extracellular K+. Also dibutyryl cyclic AMP and theophylline lacked the ability to raise [Ca2+]i beyond that obtained by glucose. The results suggest that cyclic AMP potentiates glucose-induced insulin release by sensitizing the secretory machinery to changes of [Ca2+]i rather than by increasing the cytosolic concentration of the ion.

Animals↗
PubMed1985

Effect of selective and non-selective antimuscarinics on rectosigmoid motility and gastrointestinal transit.

In 12 healthy volunteers, a rectosigmoid motility index (RSMI) was measured when either placebo, 0.5 mg atropine, or 5 mg pirenzepine was given intravenously as a single dose, double-blind, in random order after a control period of 30 min. Compared with the control period, atropine gave a significant decrease of the RSMI during the entire recorded period of 90 min, whereas pirenzepine inhibited RSMI only during the first two 15-min periods. In another series of experiments, gastrointestinal transit was assessed by means of a radiographic marker method. In healthy volunteers, gastrointestinal transit was estimated (n = 20) and gastric secretion was measured (basally and after modified sham feeding; n = 10) during oral medication with placebo, 50 mg pirenzepine twice daily, or 17.5 mg benzilonium bromide twice daily. In 10 of the volunteers gastrointestinal transit was also estimated with 35 mg benzilonium bromide twice daily, and in the other 10 volunteers with 0.6 mg L-hyoscyamine twice daily. The number of retained markers was significantly lower during pirenzepine than during L-hyoscyamine treatment. Neither dose of benzilonium bromide changed the transit of markers. Compared with non-selective antimuscarinics, the effect of pirenzepine was differential: with equipotently acid-reducing doses the decrease of the RSMI after pirenzepine lasted shorter and gastrointestinal transit was accelerated.

Adult↗
PubMed1985

Rectosigmoid motility response to beta-adrenoceptor stimulation in patients with the irritable bowel syndrome.

Patients with the irritable bowel syndrome were studied with regard to the effects of beta-adrenoceptor agonists on rectosigmoid motility. Pressure was recorded with a continuously inflated balloon in the upper rectum and recorded from a pressure catheter in the sigmoid colon. On different days the beta-2 agonist terbutaline, the beta-1 agonist prenalterol, and placebo, respectively, were administered intravenously after a control period. During each examination contractile activity was quantified for three consecutive periods of 25 min. Terbutaline in a total dose of 0.50 mg decreased sigmoid motility index significantly from 3.0 +/- 0.6 (SEM) to 1.1 +/- 0.3 kPa X min (p less than 0.01). After less than or equal to 5 mg prenalterol no significant changes of motility index were observed. After placebo an increase, although not significant, in contractile activity was seen compared with the initial control period. Rectal motility indices were low and not changed by the beta agonists. The serum concentrations of the drugs were within the therapeutic limits used in clinical practice and caused a dose-dependent increase of both systolic blood pressure and heart rate. It is concluded that beta-2 adrenoceptor stimulation significantly decreases sigmoid motility whereas the motility index seems to be unaffected by beta-1 adrenergic stimulation.

Adrenergic beta-Agonists↗
PubMed1985

Failure of beta-adrenergic stimulation to affect cholecystokinin-stimulated sigmoid motility in man.

Sigmoid motility, stimulated by the octapeptide of cholecystokinin (OP-CCK) and the effects of beta-adrenoceptor agonists, was studied in 12 healthy subjects in a randomized, double-blind fashion. Sigmoid pressure was recorded 18-20 cm from the anus, and contractile activity quantified as the area under pressure waves for three 25-min periods. OP-CCK (sincalide), 80 ng X kg-1 X h-1, was continuously infused throughout each session, resulting in a high sigmoid motility index. Preceded by a control period, terbutaline (beta-2 agonist), prenalterol (beta-1 agonist), or placebo was injected on 3 separate days. After 1 mg + 4 mg prenalterol or 0.25 mg + 0.25 mg terbutaline intravenously no significant changes in motility pattern were seen compared with the control period. Terbutaline and prenalterol infusions were followed by a dose-dependent increase of systolic blood pressure and heart rate. After placebo no effect on blood pressure or heart rate was seen. The study shows that CCK significantly enhances sigmoid motility in man and that selective beta-adrenergic agonists do not show any inhibitory influence on colonic motility stimulated with CCK. Since terbutaline inhibits sigmoid and rectal motility in man during rectal distention, it is suggested that the inhibitory effect of beta-2-adrenoceptor agonists may be dependent on the mode of background stimulation of the colon.

Adrenergic beta-Agonists↗
PubMed1985

The dual action of glucose on the cytosolic Ca2+ activity in pancreatic beta-cells. Demonstration of an inhibitory effect of glucose on insulin release in the mouse and man.

The cytosolic Ca2+ activity was measured with the fluorescent indicator quin-2 in pancreatic beta-cells obtained from obese-hyperglycemic mice. When present at a concentration of 20 mmol/l in a medium physiologically balanced in cations, glucose induced a rise of cytosolic Ca2+ after a delay of 1--3 min. At lower concentrations of extracellular Ca2+ this effect was not only prevented but the sugar promptly reduced the cytosolic Ca2+ activity. The dual effect of glucose on cytosolic Ca2+ had its counterpart in the release of insulin. Whereas 20 mmol/l of glucose stimulated the release of insulin from mouse islets previously stored in a Ca2+-deficient medium, the sugar was clearly inhibitory when present at a concentration of 6 mmol/l. Intravenous glucose tolerance tests revealed a temporary glucose depression of the serum concentrations of insulin and C-peptide in several patients with diabetes. In a mentally retarded girl with hyperinsulinemia associated with acanthosis nigricans the glucose suppression of circulating insulin was prolonged and sufficiently pronounced to suggest an almost complete inhibition of the secretory activity of the pancreatic B-cells.

Aminoquinolines↗
PubMed1984

Dual effects of glucose on the cytosolic Ca2+ activity of mouse pancreatic beta-cells.

The cytosolic Ca2+ activity of mouse pancreatic beta-cells was studied with the intracellular fluorescent indicator quin2 . When the extracellular Ca2+ concentration was 1.20 mM, the basal cytosolic Ca2+ activity was 162 +/- 9 nM. Stimulation with 20 mM glucose increased this Ca2+ activity by 40%. In the presence of only 0.20 mM Ca2+ or after the addition of the voltage-dependent Ca2+ -channel blocker D-600, glucose had an opposite and more prompt effect in reducing cytosolic Ca2+ by about 15%. It is concluded that an early result of glucose exposure is a lowering of the cytosolic Ca2+ activity and that this effect tends to be masked by a subsequent increase of the Ca2+ activity due to influx of Ca2+ through the voltage-dependent Ca2+ channels.

Animals↗
PubMed1984

Defective regulation of the cytosolic Ca2+ activity in parathyroid cells from patients with hyperparathyroidism.

The parathyroid hormone (PTH) release and cytosolic Ca2+ activity were determined in normal bovine parathyroid cells and parathyroid cells obtained from patients with hyperparathyroidism (HPT). There was a sigmoid relation between the cytosolic Ca2+ activity and the extracellular calcium concentration between 0.5 and 6.0 mmol/l. The PTH release was inhibited in parallel with the rise in the cytosolic Ca2+ activity. Both the hormone release and the cytosolic Ca2+ activity were lower in cells from human adenomas and hyperplastic glands, and in comparison with the bovine preparations these cells had higher set points for the cytosolic Ca2+ activity and PTH release. There was a close correlation between the individual set points for the cytosolic Ca2+ activity and PTH release in a material containing both normal and pathological cells. The results indicate that the abnormal PTH release characteristic of HPT is due to a defective regulation of the cytosolic Ca2+ activity.

Adenoma↗