Contractility and supersensitivity to adrenaline in dystrophic muscle.

Takamori, Masaharu

doi:10.1136/jnnp.38.5.483

Cited by 16 publications

(5 citation statements)

References 32 publications

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“…The staircase phenomenon in the ADP is absent or negative in patients with the Duchenne form of progressive muscular dystrophy ( Desmedt & Emeryk 1968) and in other types of myopathy (Meienberg & Ludin 1977). The negative staircase in dystrophic muscle was suggested to be due to a decreased active state (Takamori 1975). Also, in a boy with McArdle's disease and signs of myopathy in the EMG we found the staircase to be absent (Brandt et al 1977).…”

Section: Twitch Potentiation In Myopathymentioning

confidence: 58%

Evoked responses in normal and diseased muscle with particular reference to twitch potentiation

Krarup

1983

Acta Neurologica Scandinavica

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The compound muscle action potential and isometric twitch tension evoked by single and repetitive electrical stimuli are indicators of the number of motor units activated and of the contractile properties of the muscle. The action potentials and mechanical responses were recorded in proximal and distal muscles in patients with myasthenia gravis and myopathy and compared with findings in normal subjects. In normal muscle, at low rates of stimulation (2-3 s-1) the decrement was at most 5% in the action potential and 15-24% in the twitch tension. Tetanic stimuli (50 s-1) were unsuitable for diagnostic purposes because of movement artefact. In patients with myasthenia gravis, the incidence and size of the decrement of evoked responses were greater in the platysma than in the elbow flexors and the adductor pollicis (ADP) muscles. The 2-3 times greater post-tetanic facilitation (PTF) of the action potential in the platysma than in extremity muscles also indicates a more severe functional block in facial muscle. The PTF is an indicator of recruitment of blocked fibres. The maximal decrement was grossly related to the titre of antibodies against the acetylcholine receptor. To reveal failure of neuromuscular transmission in patients with myasthenia gravis without a decrement, a small dose of d-tubocurarine (0.2 mg in 30 ml of saline) was injected i.v. in the upper arm in a regional curare test. The sensitivity was greater in patients with myasthenia gravis than in controls and in patients with myopathy. Potentiation of twitch tension reflects contractile properties. In normal muscle twitch potentiation in the staircase (1-3 s-1, 100 s in duration) and after tetanus (50 s-1, 1.5 s in duration) was 2-3 times greater in the platysma than in the elbow flexors and ADP, presumably related to the greater proportion of fast-twitch fibers in facial muscle. The amplitude of the action potential and the twitch tension varied proportionally with the number of fibers activated and the difference in the decrements of the action potential and the twitch during the staircase in some patients with myasthenia gravis showed that the staircase phenomenon was diminished suggesting abnormalities in the excitation-contraction coupling. The diminution of the staircase and post-tetanic potentiation (PTP) in myopathy also indicates impairment of the excitation-contraction coupling. In rats with severe chronic myasthenia gravis, the staircase and PTP were decreased even when the failing neuromuscular transmission was circumvented by applying direct stimuli to the extensor digitorum longus muscle (EDL).

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Section: Twitch Potentiation In Myopathymentioning

confidence: 58%

Evoked responses in normal and diseased muscle with particular reference to twitch potentiation

Krarup

1983

Acta Neurologica Scandinavica

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“…That the lipid abnormality may extend to plasma membranes of other tissues is suggested by the findings of similar enzyme changes in erythrocytes from dystrophic patients (Chattopadhyay & Brown, 1972; Mawatari et al, 1976). Altered hormonal responses in dystrophic patients have been reported (Beckmann, 1974;Takamori, 1975;Malarkey & Mendell, 1976).…”

Section: Componentmentioning

confidence: 89%

Skeletal-muscle sarcolemma from normal and dystrophic mice. Isolation, characterization and lipid composition

Kretser¹,

Livett²

1977

Biochemical Journal

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1. Mouse skeletal-muscle sarcolemma was isolated, and the preparations obtained from normal mouse muscle and from muscle of mice with hereditary muscular dystrophy were characterized with respect to appearance under the optical and electron microscopes, distribution of marker enzymes, histochemical properties and biochemical composition. 2. The sarcolemmal membranes from normal and dystrophic muscle were subjected to detailed lipied analysis. Total lipid content was shown to increase in sarcolemma from dystrophic mice as a result of a large increase in neutral lipid and a smaller increase in total phospholipids. Further analysis of the neutral-lipid fraction showed that total acylglycerols increased 6-fold, non-esterified fatty acid 4-fold and cholesterol esters 2-fold, whereas the amount of free cholesterol remained unchanged in sarcolemma from dystrophic muscle. Significant increases were found in lysophosphatidylcholine, phosphatidylcholine and phosphatidylethanolamine in dystrophic-muscle sarcolemma; however, the relative composition of the phospholipid fraction remained essentially the same as in the normal case. 3. The overall result of alterations in lipid composition of the sarcolemma in mouse muscular dystrophy was an increase in neutral lipid compared with total phospholipid, and a 4-fold decrease in the relative amount of free cholesterol in the membrane. The possible impact of these changes on membrane function is discussed.

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“…The direct action of serotonin on the polarisation of the muscle fibre membrane (Koketsu and Shirasawa, 1974) may also play a role in this postsynaptic effect. Measuring the isometric twitch, tetanus, and their differentials, the effect of serotonin on muscle contraction was studied on the basis of the concept of the active state (Sandow, 1970;Takamori et al, 1971;Close, 1972;Takamori, 1975). Serotonin caused a reduction in twitch tension (Pt), mainly associated with a decrease in the acceleration of twitch development (d2Pt/dt2, active state intensity of shortening; Table) without change in the evoked muscle action potential (Figs.…”

Section: Discussionmentioning

confidence: 99%

“…The analysis of muscle contraction was done on the basis of the concept of the active state. Measurements and the active state properties were reported elsewhere (Takamori et al, 1971;Takamori, 1975), and are summarised in the Table. Two types of experimental blockade of the neuromuscular transmission were prepared by means of intravenous injection of 6.7% magnesium sulphate and 0.03 % D-tubocurarine chloride through a cannula in an ear vein, respectively. In each experimental state, the drug was given until the amplitude of the muscle action potential evoked by nerve stimulation was reduced to about 50 % of the original amplitude; the amplitude was kept at this level by continuous intravenous infusion using a motorised syringe.…”

Section: Methodsmentioning

confidence: 99%

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Nerve, muscle, and serotonin.

Takamori¹

1977

Journal of Neurology, Neurosurgery & Psychiatry

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SUMMARY Effects of serotonin on neuromuscular transmission and muscle contraction were studied in the tibialis anterior of rabbits. Serotonin antagonised the Mg++-induced block of transmission, and also provided dual effects on the curare-induced block, anti-curare phase followed by curare-potentiating phase. Independent of transmission processes, serotonin caused a reduction in twitch tension, mainly associated with decreased acceleration of twitch development. These serotonin actions were independent of vascular changes; pharmacological mechanisms are discussed in comparison with those of adrenaline and isoprenaline. A possible role of serotonin in causing a myopathy is proposed.A relationship between mammalian skeletal muscle and biogenic amine metabolism has been debated in relation to the pathogenesis of human muscular dystrophies. Abnormal contractile response to adrenaline (Takamori, 1975) and impaired activation of adenyl cyclase by adrenaline (Mawatari et al., 1974) suggest that adrenaline is implicated in abnormalities of the sarcoplasmic reticulum and plasma membrane in dystrophic muscles. Serotonin (5-hydroxytryptamine) is also one of the amines whose role is debated. It has been reported that an experimental myopathy similar to Duchenne muscular dystrophy was produced in the rat by ligation ofthe abdominal aorta and subsequent administration of serotonin (Mendell et al., 1971(Mendell et al., , 1972. It was presumed that the pargylineinduced myopathy, a model with histopathological features of Duchenne muscular dystrophy, was caused by an increased level of noradrenaline leading to excessive release of acetylcholine, or to an increased level of serotonin (Yu etal., 1974). Independent of vascular changes, Patten et al. (1974) demonstrated serotonin-induced depression of isometric twitch in rat skeletal muscles, and Meltzer (1976) suggested a direct effect of serotonin on rat skeletal muscles in causing myopathy. The present study attempts further to evaluate serotonin actions on neuromuscular transmission and muscle contraction. Investigations were performed in comparison with sympathomimetic amines and their antagonists, the pharmacological actions of which in the neuromuscular system are well known (Bowman and Nott,

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Contractility and supersensitivity to adrenaline in dystrophic muscle.

Cited by 16 publications

References 32 publications

Evoked responses in normal and diseased muscle with particular reference to twitch potentiation

Evoked responses in normal and diseased muscle with particular reference to twitch potentiation

Skeletal-muscle sarcolemma from normal and dystrophic mice. Isolation, characterization and lipid composition

Nerve, muscle, and serotonin.

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