Potassium in different layers of isolated diaphragm

Creese, R.

doi:10.1113/jphysiol.1960.sp006568

Cited by 8 publications

(8 citation statements)

References 12 publications

(41 reference statements)

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“…The largest part of this work has been on the muscles of frog, and relatively little attention has been paid to mammalian tissues other than diaphragm (Creese, 1954(Creese, , 1960. The present study extends some earlier work (McLennan, 1955) with mammalian skeletal muscle, and compares also the behaviour of normal tissues and those derived from animals which had developed an inherited muscular dystrophy.…”

supporting

confidence: 62%

“…The effect of inter-fibre diffusion on the equilibration of the cellular K is less certain. In earlier experiments on larger muscles, but incubated at a lower temperature (200 C), there was no detectable effect of muscle thickness on the exchange (McLennan, 1955); on the other hand Creese (1960) had evidence that the exchange may be diminished by intercellular diffusion, and the effect would be more pronounced at the higher temperature used here when the exchange process is more rapid. Since the model used for 330 K EXCHANGE IN MUSCLE the analysis of the present results requires that the exchange must follow diffusion laws, an intercellular diffusion could not be distinguished from it.…”

Section: Discussionmentioning

confidence: 94%

“…Harris & Sjodin (1961) have shown that this difficulty does not arise with the present model in which the 'membrane' is allowed to have a definite capacity for K, for the diffusion of an ion through the ion-exchange layer requires a series of exponential terms to describe it. Creese (1960) has shown that, in isolated diaphragms, an hypoxia of the fibres in the centre of the tissue can result in a curve for outward movement of K which is fitted by two exponential terms. However, this finding was associated with a net loss of K from the tissue, and this situation (in solutions with Ke > 6 mM) did not arise in the present experiments.…”

Section: Discussionmentioning

confidence: 99%

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The transport of potassium in normal and dystrophic mouse muscle

Burr¹,

McLennan²

1961

The Journal of Physiology

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The kinetics of movement of cations between muscle cells and their environment has been the subject of much work in recent years. The largest part of this work has been on the muscles of frog, and relatively little attention has been paid to mammalian tissues other than diaphragm (Creese, 1954, 1960). The present study extends some earlier work (McLennan, 1955) with mammalian skeletal muscle, and compares also the behaviour of normal tissues and those derived from animals which had developed an inherited muscular dystrophy. METHODS The mice used were from a pure strain maintained at the University of British Columbia derived from the Bar Harbour 129 strain. This strain develops a disorder of muscle transmitted as an autosomal recessive trait which closely resembles human progressive muscular dystrophy both genetically and histologically (Michelson, Russell & Harman, 1955). Litter-mates which did not develop the condition provided normal controls. All experiments were carried out in vitro with m. gastrocnemius weighing 15-25 mg. The tissues were excised, weighed on a small torsion balance and incubated by allowing them to float freely in approx. 50 ml. of the desired saline medium in a bath set at 350 C. To measure the uptake of labelled ion the muscles were removed at intervals from the incubation medium, rinsed for exactly 1 min in a solution of identical ionic composition but without radioactive tracer, and placed beneath an end-window Geiger-Muller tube. Care was taken to ensure that the geometry of the relationship between tissue and detector was the same for each measurement. After counting for three 1 min periods the tissues were returned to the incubation medium. At the end of the experiment the tissue was dissolved in a few drops of concentrated nitric acid, diluted to 2 ml. and the radioactivity of the solution compared to that of a dilution of the incubating fluid. In this way a cross-relationship between K in the tissue and counts per minute could be established. The same solution of the muscle was used for analysis of the total tissue Na and K by the use of a flame photometer. The isotope used was 42K. Its disintegration was detected with the aid of a Geiger-Miller tube connected to a scaler unit. All radioactive counts were corrected for decay, background and resolution time of the counter-scaler combination. The solutions used for incubation were variants upon one containing (m-mole/l.): Na 144, K6, Ca 2, Mg 1, Cl 134, HCO3 20, S04 1, glucose 10, and vigorously bubbled with 95 % 02+5 % CO2. That this condition was adequate for maintenance of the normal metabolism

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supporting

confidence: 62%

Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

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The transport of potassium in normal and dystrophic mouse muscle

Burr¹,

McLennan²

1961

The Journal of Physiology

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“…The deterioration of the isolated muscles was attributed, at least in part, to impaired aerobic metabolism. Creese (1960) and Creese & Northover (1961) have followed the changes in intracellular Na+ and K+ in the isolated rat diaphragm and have shown that these concentrations can only be maintained at control levels by using solutions with a high K+ content and fortified with serum or proteins. Even then the muscle is very sensitive to changes in oxygen supply or stimulation frequency.…”

Section: Discussionmentioning

confidence: 99%

A Comparison of the Responses of the Tenuissimus Muscle to Neuromuscular Blocking Drugs in Vivo and in Vitro

Maclagan

1962

British Journal of Pharmacology and Chemotherapy

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In view of the differing responses to decamethonium which have been reported for the isolated tenuissimus muscle on the one hand and the tibialis muscle of the cat on the other hand, the responses of the tenuissimus muscle to neuromuscular blocking drugs were studied both in vivo and in vitro and compared with those of the tibialis anterior muscle. In both muscles in vivo, the block produced by decamethonium had all the well‐known characteristics of blockade due to long‐lasting depolarization, independent of the number of doses given. However, when the tenuissimus muscle was studied in vitro its responses were considerably altered. When decamethonium was left in contact with the isolated muscle, maximum paralysis developed quickly, but then the muscle recovered despite the continued presence of the drug in the bath. This contrasts with the effect obtained in vivo, where a steady application of decamethonium produced steady blockade. This spontaneous recovery in vitro occurred to a smaller extent with each successive dose. In addition, the usual antagonism between depolarizing and competitive drugs was only seen during the earlier part of an experiment and rarely occurred after several doses. It is suggested that the differences between in vivo and in vitro responses of the tenuissimus muscle to decamethonium could be due to detrimental changes in ionic concentration gradients resulting from immersion in an artificial fluid.

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“…It is well established that hypoxia reduces the active transport of sodium and potassium ions in nerve (Shanes & Berman, 1955;Connelly, 1959;Ito & Oshima, 1964) and in the rat diaphragm muscle a similar depression may be assumed from the loss of potassium ions and gain of sodium ions which occurs in anoxic muscle fibres (Creese, 1954(Creese, , 1960. Presumably this depression of active transport is responsible not only for the abolition of PTP (Figs.…”

mentioning

confidence: 86%

The effects of hypoxia on neuromuscular transmission in a mammalian preparation

Hubbard¹,

Løyning²

1966

The Journal of Physiology

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SUMMARY1. The rat diaphragm-phrenic nerve preparation in vitro failed to contract in response to nerve impulses after [10][11][12][13][14][15][16][17][18][19][20] 5. There was an increase in the post-synaptic sensitivity to carbamylcholine after 20 min hypoxia which was sufficient to explain the increase in m.e.p.p. amplitude. Other post-synaptic changes were a fall in membrane potential (average 6 mV after 20 min) and a fall in membrane resistance after 30-60 min exposure to hypoxia.6. The effects of hypoxia upon neuromuscular transmission were partially explained by reduction of active transport of sodium and potassium ions and consequent depolarization of nerve and muscle.

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Potassium in different layers of isolated diaphragm

Cited by 8 publications

References 12 publications

The transport of potassium in normal and dystrophic mouse muscle

The transport of potassium in normal and dystrophic mouse muscle

A Comparison of the Responses of the Tenuissimus Muscle to Neuromuscular Blocking Drugs in Vivo and in Vitro

The effects of hypoxia on neuromuscular transmission in a mammalian preparation

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