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T Clausen

Publications and source records attributed to T Clausen.

At least 109 records · Page 6Linked to original sources
PubMed1993

Changes in K+, Na+ and calcium contents during in vivo stimulation of rat skeletal muscle.

The effects of in vivo stimulation via the sciatic nerve on Na+, K+ and calcium contents in slow-twitch and fast-twitch muscles were compared. Whereas intermittent stimulation for 24 h at 20 Hz caused only minor changes in soleus (SOL), a considerable loss of K+ (around 24%) and gain of Na+ (around 84%) was observed in extensor digitorum longus (EDL) and tibialis anterior (TA) muscles. These changes could be detected within 0.5 h and a plateau was maintained from 2 to 24 h. Total calcium content increased progressively, reaching values 245 and 382% above the control level in EDL and TA muscle, respectively, after 24 h of 20 Hz stimulation. Whereas the Na+ and K+ content recovered within a few hours, calcium content did not return towards control level until after 48 h of rest. In a pilot study performed with continuous stimulation at 10 Hz, the changes in Na+ and K+ contents in SOL, EDL and TA muscle were comparable to those at 20 Hz. The concentration of the Na(+)-K+ pumps was highest in the fast-twitch EDL and TA muscles and was unaffected by 10 Hz stimulation. It is concluded that a stimulation pattern leading to a rise in intracellular Na+ and a loss of K+ may cause a marked accumulation of calcium. These events seem to be related to insufficient activation of the Na-K+ pump rather than to variations in the total Na(+)-K+ pump capacity.

Adenosine Triphosphate↗
PubMed1993

Na(+)-K+ pump stimulation elicits recovery of contractility in K(+)-paralysed rat muscle.

1. This study explores the role of active electrogenic Na(+)-K+ transport in restoring contractility in isolated rat soleus muscles exposed to high extracellular potassium concentration ([K+]o). This was done using agents (catecholamines and insulin) known to stimulate the Na(+)-K+ pump via different mechanisms. 2. When exposed to Krebs-Ringer bicarbonate buffer containing 10 mM K+, the isometric twitch and tetanic force of intact muscles decreased by 40-69%. The major part of this decline could be prevented by the addition of salbutamol (10(-5) M). In the presence of 10 mM K+, force could be restored almost completely within 5-10 min by the addition of salbutamol or adrenaline and partly by insulin. 3. In muscles exposed to 12.5 mM K+, force declined by 96%. Salbutamol (10(-5) M), adrenaline (10(-6) M) and insulin (100 mU ml-1) produced 57-71, 61-71 and 38-47% recovery of force within 10-20 min, respectively. The effects of these supramaximal concentrations of salbutamol and insulin on force recovery were additive. Salbutamol and adrenaline produced significant recovery of contractility at concentrations down to 10(-8) M (P < 0.005). 4. In soleus, the same agents stimulated 86Rb+ uptake and decreased intracellular Na+. These actions reflect stimulation of active Na(+)-K+ transport and both showed a highly significant correlation to the recovery of twitch as well as tetanic force (r = 0.80-0.88; P < 0.001). 5. The force recovery induced by salbutamol, adrenaline and insulin was suppressed by pre-exposure to ouabain (10(-5) M for 10 min or 10(-3) M for 1 min) as well as by tetrodotoxin (10(-6) M). 6. The observations support the conclusion that the inhibitory effect of high [K+]o on contractility in skeletal muscle can be counterbalanced by stimulation of active electrogenic Na(+)-K+ transport, the ensuing increase in the clearance of extracellular K+ and in the transmembrane electrochemical gradient for Na+.

Albuterol↗
PubMed1993

Calcitonin gene-related peptide stimulates active Na(+)-K+ transport in rat soleus muscle.

Calcitonin gene-related peptide (CGRP) is found in a wide variety of tissues, including sensory and motor nerve endings in skeletal muscle. After intense electrical stimulation or K(+)-induced depolarization, CGRP can be released from nerve terminals and bound to receptors on sarcolemma. We show here that CGRP (rat and human) and salmon calcitonin stimulate 22Na extrusion and the influx of 86Rb and 42K in isolated rat soleus muscle. This leads to a pronounced (up to 56%) decrease in intracellular Na+, a minor increase in intracellular K+, and hyperpolarization. All these effects were blocked by ouabain or cooling, indicating that they reflect an acute stimulation of active electrogenic Na(+)-K+ transport. Capsaicin, which induces release of CGRP from sensory nerve endings, was found to exert similar effects on Na(+)-K+ transport. Various Na(+)-K+ pump-stimulating agents have been shown to counteract the inhibitory effect of a high extracellular concentration of K+ ([K+]o) on muscle contractility (4, 20). CGRP and capsaicin were likewise found to improve contractile performance of muscles inhibited by high [K+]o, and these effects were blocked by ouabain. CGRP might play a role in the maintenance of Na(+)-K+ gradients and excitability during intensive muscle work, known to be associated with an acute rise in the interstitial K+ concentration.

Animals↗
PubMed1993

Correlation between magnesium and potassium contents in muscle: role of Na(+)-K+ pump.

In young rats fed a Mg(2+)-deficient diet for 3 wk, Mg2+ and K+ contents in soleus and extensor digitorum longus muscles were significantly reduced and closely correlated. In isolated soleus muscles, Mg2+ depletion induced an even more pronounced loss of K+, and Mg2+ and K+ contents were correlated over a wide range (r = 0.95, P < 0.001). Extracellular Mg2+ (0-1.2 mM) caused no change in total or ouabain-suppressible 86Rb influx. After long-term incubation in Ca(2+)-Mg(2+)-free buffer with EDTA and EGTA, cellular Mg2+ and K+ contents were reduced by 35 and 15%, respectively, without any reduction in ATP and total or ouabain-suppressible 86Rb influx. In Mg(2+)-depleted muscles 42K efflux was increased by up to 42%, and repletion with Mg2+ produced a graded decrease. We conclude that Mg2+ and K+ contents are closely correlated in muscles Mg2+ depleted in vivo or in vitro and that neither extracellular nor moderate intracellular Mg2+ depletion affects total or Na(+)-K+ pump-mediated K+ influx. The reduced K+ content may rather be related to increased K+ efflux from the muscles.

Animals↗
PubMed1993

Factor analysis of the WAIS-R and Verbal Memory and Visual Memory Indices of the Wechsler Memory Scale--Revised, for a vocational rehabilitation sample.

Few empirical studies have examined factor structures of responses of vocationally impaired persons, and those studies have drawn only on aptitude scores (Wechsler Adult Intelligence Scale--Revised: WAIS--R). Results have been inconclusive as to whether a two- or three-factor solution is more appropriate. The present work examined the factor scores of a vocational rehabilitation sample of 54 adults who had been given the WAIS--R and the Verbal Memory and Visual Memory Indices of the Wechsler Memory Scale--Revised. Analysis indicated that combining data from the two tests yields a viable three-factor solution which may contribute to the refinement of intervention strategies for vocationally vulnerable adults.

Accidents, Occupational↗
PubMed1992

Effects of reduced joint mobility and training on Na,K-ATPase and Ca-ATPase in skeletal muscle.

In guinea pigs, the ankle joint was partly immobilized in a position reducing dorsiflection to 105 degrees (as compared to the normal value of 30 degrees). When compared with the contralateral unrestrained leg, this led to a significant atrophy and a decrease in contractile force (-23%) of the gastrocnemius muscle. This was associated with a significant decrease in the total concentration of [3H]ouabain binding sites in gastrocnemius and plantaris muscle reaching minimum (-19% and -23%) after 3 weeks, but no evidence of degenerative changes. Total contents of Ca and Ca-ATPase were increased by 27% and 22%, respectively. After 4 to 5 weeks of reduced mobility, the concentration of [3H]ouabain binding sites in gastrocnemius muscle returned to control level. The lowest concentration of [3H]ouabain binding sites reached during reduced mobility was 258 +/- 13 pmol/g wet wt., and the maximum value attained following 3 weeks of reduced mobility and 3 weeks of training by running was 498 +/- 25 pmol/g wet wt., i.e, 93% higher. In soleus, training produced an increase of 25%. Clinically, it is important to realize that movable braces cannot prevent the development of muscular atrophy. The observed spontaneous recovery of the Na,K-pump concentration may partly explain why patients using movable casts show a better capacity for physical performance than those treated with complete immobilization. In conclusion, the total concentration of Na,K-pumps in guinea pig skeletal muscle undergoes downregulation and upregulation as a function of contractile activity as well as muscle length under conditions mimicking the constraints on mobility frequently used in the clinical treatment of lesions.

Animals↗
PubMed1992

Activation of the Na-K pump by intracellular Na in rat slow- and fast-twitch muscle.

Experiments were performed on isolated rat soleus (slow-twitch) and extensor digitorum longus (EDL) (fast-twitch) muscle of 4-week-old rats. In soleus muscle, electrical simulation at 2 Hz for 5 min increased the ouabain-suppressible 86Rb+ uptake by 138%, without significant changes in intracellular Na+ content or Na+/K+ ratio. In EDL muscle, the ouabain-suppressible 86Rb+ uptake was stimulated by only 58%, whereas intracellular Na+ content and Na+/K+ ratio were increased by around 70%. Na(+)-loading of the muscles by exposure to K(+)-free or K(+)-Ca(2-)-Mg(2+)-free buffer stimulated the ouabain-suppressible 86Rb+ uptake in the two muscles to roughly the same extent, but in EDL muscle this was associated with a more than twofold larger increase in Na+/K+ ratio. When the Na+ influx was increased by exposure to veratridine similar results were obtained. Graded variation in intracellular Na+ content was achieved by exposure to monensin. In soleus muscle, a 25% increase in intracellular Na+/K+ ratio resulted in a doubling of the ouabain-suppressible 86Rb+ uptake, whereas a doubling of the Na(+)-K+ transport rate in EDL muscle required a 140% increase in Na+/K+ ratio. The results indicate that in soleus muscle the Na+/K+ pump is much more sensitive to changes in intracellular Na+ content than in EDL muscle. This might explain the larger activation of the Na(+)-K+ pump in slow-twitch muscle during electrical stimulation and might be of significance for the activation of the Na(+)-K+ pump in vivo during work.

Adenosine Triphosphate↗
PubMed1992

Potassium and sodium transport and pH regulation.

The excitatory and metabolic events in nervous tissue lead to localized increases in extracellular potassium (K+) and intracellular hydrogen (H+) and calcium (Ca2+) ion concentrations. Even more pronounced increases are seen under pathological conditions and may interfere with the maintenance of cellular function and structure. Most presentations on the second day focused on these processes and the mechanisms for the clearance of K+, H+, and Ca2+ from intra- or extra-cellular compartments. The essential role of glial cells was a returning theme. Extracellular K+ is transported into cells by the Na-K pump and by two other processes, Na-K-Cl2 cotransport and spatial buffering, which both depend on the operation of the Na-K pump. The clearance of H+ from the cytoplasm and into the extracellular space is mediated by Na+ gradient dependent processes, Na+/H+ antiport, Cl-/HCO3- exchange, and Na(+)-HCO3- cotransport. Also the clearance of cytoplasmic Ca2+ is to a large extent mediated by a Na+ gradient dependent process, the Na+/Ca2+ antiport. There is a wide divergence between the rates of Na-K pump mediated K+ influx measured in various cultures of glial and neuronal cells. There is a considerable need for systematic comparison between the functional capacity and the concentration of Na-K pumps in cell cultures and intact nervous tissue. It has not yet been ascertained whether K+ transport as measured in cultured astrocytes is representative for K+ transport in the in situ functioning astrocyte. In astrocytes, glutamate was shown to elicit a rapid intercellular propagation of a rise in cytoplasmic Ca2+.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1991

[Tracheobronchial tumors treated with laser. 7-year experiences at Aker hospital].

The first Nd-YAG laser treatment for endoluminal airway obstruction in Norway was performed at Aker Hospital in November 1983. During the ensuing seven years 68 patients have been treated, involving altogether 172 procedures. During the early years a flexible bronchoscope was used to guide the flexible laser probe, in later years the usual practice has been to use the rigid bronchoscope, 54 patients were treated for malignant tumour, three for semi-malignant and 11 for benign tumour. In general, the best results were achieved with a proximal location of the tumour. Two patients died during the procedure from hypoxia, and one patient died from hemoptysis on the fifth day after operation. Based on retrospective studies of the clinical journal and the results from postmortem examination of 97 consecutive patients who died from pulmonary carcinoma, we anticipated that six of these patients would have benefited from laser treatment on at least one occasion during their disease. In Norway, with an incidence of approximately 400 cases of pulmonary carcinomas each year per million inhabitants, we estimate the need of lung laser procedures to be 25 per million each year.

Adolescent↗
PubMed1991

Effects of magnesium and terbutaline on contractility and K+ uptake in isolated human uterine muscle.

Mg++ (3 and 6 mmol/L), the beta 2-adrenergic agonist terbutaline (1 and 10 mumol/L), and dibutyryl cyclic adenosine 5'-monophosphate (0.1 and 1 mmol/L) suppressed spontaneous activity and the increase in contractile activity induced by ouabain or K(+)-free buffer in isolated human pregnant myometrium. The ouabain-suppressible rubidium 86 or potassium 42 uptake was unaffected by the presence of Mg++ (3 and 6 mmol/L), the beta 2-adrenergic agonist terbutaline (1 and 10 mumol/L), or dibutyryl cyclic adenosine 5'-monophosphate (1 mmol/L). However, loading of the strips with Na+ and incubation in high K+ induced a fivefold increase in rubidium 86 uptake. On the basis of these flux rates, our previous data on the total concentration of sodium-potassium pumps in the human myometrium, and an estimated maximum transport rate of the sodium-potassium pump of 8900 K+ ions per minute at 30 degrees C, it could be calculated that the sodium-potassium pump in the Na(+)-loaded strips reached around 80% of its maximal rate. Taken together, these results showed that the relaxant effects of Mg++, terbutaline, and dibutyryl cyclic adenosine 5'-monophosphate on human myometrium are not due to a stimulation of active sodium-potassium transport.

Biological Transport↗
PubMed1991

Effects of magnesium and zinc deficiencies on growth and protein synthesis in skeletal muscle and the heart.

The effects of magnesium or zinc deficiency on growth, tissue contents of Mg or Zn and protein synthesis have been compared in 4-13-week-old rats. When maintained on Mg-deficient fodder (1.6 mmol/kg) or Zn-deficient fodder (27 mumol/kg) rats showed a reduced weight gain, whereas repletion caused increased growth rates. Pair-feeding experiments showed that this could not be attributed to reduced energy intake only. In rats maintained on Mg-deficient fodder for 14 d [3H] leucine incorporation into skeletal muscle and the heart was reduced by 24-38% compared with pair-fed controls (P less than 0.001-0.002). The incorporation of [3H]phenylalanine was reduced by 19-31%. Tissue Mg contents, however, were only reduced by 6-7% (not significant). The pair-fed rats showed no reduction in the [3H]leucine incorporation compared with ad lib.-fed animals. In rats maintained on Zn-deficient fodder for 15 d [3H]leucine incorporation into skeletal and heart muscle was reduced by 57-64% compared with pair-fed controls. The pair-fed rats showed no reduction in the [3H]leucine incorporation compared with ad lib. fed animals. In the Zn-deficient animals the content of Zn was not reduced in the skeletal muscles, whereas there was a small (15%) but significant loss of Zn in the heart. In another experiment, Zn depletion for 17 d caused a reduction in [3H]leucine incorporation of 35-41%. After 5 d of Zn repletion this defect was restored, and the [3H]leucine incorporation was above control level in the skeletal muscles. It is concluded that the intact organism is very sensitive to dietary Mg or Zn deficiency, and that the reduced growth and protein synthesis cannot easily be attributed to the reduction of tissue Mg or Zn content per se. This points to the existence of other control mechanisms mediating down-regulation of growth and protein synthesis in response to reduced dietary supplies and the ensuing drop in the plasma concentrations of Mg and Zn.

Animals↗
PubMed1991

Role of insulin-like growth factor-1 and growth hormone in growth inhibition induced by magnesium and zinc deficiencies.

Nutritional deficiencies of magnesium or zinc lead to a progressive and often marked growth retardation. We have evaluated the effect of Mg and Zn deficiency on growth, serum insulin-like growth factor-1 (s-IGF-1), growth hormone (s-GH) and insulin (s-insulin) in young rats. In 3-week-old rats maintained on Mg-deficient fodder for 12 d the weight gain was reduced by about 34%, compared with pair-fed controls. This was accompanied by a 44% reduction in s-IGF-1, while s-insulin showed no decrease. After 3 weeks on Mg-deficient fodder, growth had ceased while serum Mg (s-Mg) and s-IGF-1 were reduced by 76 and 60% respectively. Following repletion with Mg, s-Mg was completely normalized in 1 week, and s-IGF-1 reached control level after 2 weeks. Growth rate increased, but the rats had failed to catch up fully in weight after 3.5 weeks. Absolute and relative pair-feeding were compared during a Mg repletion experiment. Absolute pair-fed animals were given the same absolute amount of fodder as the Mg-deficient rats had consumed the day before. Relative pair-fed animals were given the same amount of fodder, on a body-weight basis, consumed in the Mg-deficient group the day before. In a repletion experiment the two methods did not differ significantly from each other with respect to body-weight, muscle weight, tibia length and s-IGF-1, although there was a tendency towards higher levels in the relative pair-fed group. The peak in s-GH after growth hormone-releasing factor 40 (GRF 40) was 336 (SE 63) micrograms/l in 5-week-old rats that had been Mg depleted for 14 d, whereas age-matched control animals showed a peak of 363 (SE 54) micrograms/l (not significant). In 3-week-old rats maintained on Zn-deficient fodder for 14 d weight gain was reduced by 83% compared with pair-fed controls. Serum Zn (s-Zn) and s-IGF-1 were reduced by 80 and 69% respectively, while s-insulin was reduced by 66%. The Zn-deficient animals showed a more pronounced growth inhibition than that seen during Mg deficiency and after 17 d on Zn-deficient fodder s-IGF-1 was reduced by 83%. Following repletion with Zn, s-Zn was normalized and s-IGF-1 had increased by 194% (P less than 0.05) after 3 d. s-IGF-1, however, was not normalized until after 2.5 weeks of repletion.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

K(+)-induced inhibition of contractile force in rat skeletal muscle: role of active Na(+)-K+ transport.

During excitation, K+ is lost from the working muscle fibers, and interfiber K+ may reach 10-15 mM. This, in turn, may lead to depolarization and impairment of contractile performance. The significance of elevated interfiber K+ was assessed by exposing rat muscles of uniform size (25 mg) to buffer containing 12.5-15 mM K+ and studying the decline in contractile performance and its recovery following restoration of the K+ concentration of the standard buffer (5.9 mM). When active Na(+)-K+ transport was partially inhibited by ouabain (10(-6)-10(-5) M leading to relative occupancies of 28 and 84%, respectively), the decrease in force development induced by high K+ in soleus was considerably accelerated and recovery was delayed. Conversely, when active Na(+)-K+ transport was stimulated by epinephrine, the beta 2-agonist salbutamol, or insulin, the exposure to high K+ gave a much slower decline in force. The time until full inhibition was closely correlated to the rate of Na(+)-K+ pump-mediated 86Rb uptake (r = 0.98; P less than 0.005). Significant retardation of K(+)-induced force decline could be detected down to 10(-8) M epinephrine or salbutamol. After restoration of 5.9 mM K+, recovery was promoted by epinephrine and salbutamol but not by insulin. In extensor digitorum longus muscle, insulin reduced the rate of force decline induced by exposure to 15 mM K+. The results indicate that the Na(+)-K+ pump plays a major role in the maintenance of contractility during the physiological acute exposure to high extracellular K+ associated with muscle work.

Adenosine Triphosphate↗
PubMed1990

Co-existence of myosin heavy chain I and IIa isoforms in human skeletal muscle fibres with endurance training.

The myosin heavy chain (MHC) composition of single fibres from m. vastus lateralis was analysed by one-dimensional electrophoresis and immunoblotting in three groups of young men with distinct difference in physical activity patterns. No major co-existence of MHC isoforms was found in the group with some daily physical activity. In the very sedentary group, however, 19 +/- 5% (P less than 0.05) of the fibres exhibited coexistence of MHC type IIa and IIb. Further, in the endurance trained group co-existence of MHC type I and IIa was manifested in 36 +/- 4% (P less than 0.05) of the fibres. Disuse and extreme usage of muscle both give rise to an elevation in co-expression of MHC isoforms in single muscle fibres but of markedly different combination of isoforms.

Adult↗
PubMed1989

Quantitative determination of Ca2+-dependent Mg2+-ATPase from sarcoplasmic reticulum in muscle biopsies.

The possibility of quantifying the total concentration of Ca2+-dependent Mg2+-ATPase of sarcoplasmic reticulum was investigated by measurement of the Ca2+-dependent steady-state phosphorylation from [gamma-32P]ATP and the Ca2+-dependent 3-O-methylfluorescein phosphatase (3-O-MFPase) activity in crude muscle homogenates. The Ca2+-dependent phosphorylation at 0 degree C (mean +/- S.E.) was 40.0 +/- 2.5 (n = 6) and 6.2 +/- 0.7 (n = 4) nmol/g wet wt. in rat extensor digitorum longus (EDL) and soleus muscle, respectively (P less than 0.001). The Ca2+-dependent 3-O-MFPase activity at 37 degrees C was 1424 +/- 238 (n = 6) and 335 +/- 56 (n = 4) nmol/min per g wet wt. in rat EDL and soleus muscle, respectively (P less than 0.01). The molecular activity calculated from these measurements amounted to 35 +/- 5 min-1 (n = 6) and 55 +/- 10 min-1 (n = 4) for EDL and soleus muscle respectively. These values were not different from the molecular activity calculated for purified Ca2+-ATPase (36 min-1). The Ca2+-dependent 32P incorporation in soleus muscle decreased in the order mice greater than rats greater than guinea pigs. In EDL muscles from hypothyroid rats at a 30% reduction of the Ca2+-dependent phosphorylation was observed. The Ca2+-dependent phosphorylation in vastus lateralis muscle from three human subjects amounted to 4.5 +/- 0.8 nmol/g wet wt. It is concluded that measurement of the Ca2+-dependent phosphorylation allows rapid and reproducible quantification of the concentration of Ca2+-dependent Mg2+-ATPase of sarcoplasmic reticulum. Since only 20-60 mg of tissue is required for the measurements, the method can also be used for biopsies obtained in clinical studies.

Animals↗