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Results for “Muscle Relaxation”

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At least 19 recordsLinked to original sources
PubMed1978

[Muscle relaxation and muscle spindle adaptation].

In experiments on deefferented m. triceps surae of the cats, the unequal correlation between speed of muscle relaxation during interval from 2.5 to 40 sec after the beginning of static stretch and the rate of adaptation of three functionally different groups of muscle spindles, was revealed. The dependence of the adaptation of muscle spindle endings on relaxation of both extra-and intrafusal muscle fibers, is discussed.

Adaptation, Physiological↗
PubMed1976

Computer controlled muscle relaxation: a comparison of four muscle relaxants in the sheep.

Computer control of anaesthesia has been extended to include muscle relaxant drugs. Injection of d-tubocurarine, gallamine, alcuronium or pancuronium was controlled by computer to reduce the integrated electromyogram to a preset level (40 per cent of control) for one hour. A programmed level of muscle paralysis is therefore possible for use in physiological and pharmacological experiments, and in clinical practice where precise control of the degree of paralysis together with minimal dosage is advantageous.

Alcuronium↗
PubMed1990

[The effect of flupirtine, various analgesics and muscle relaxants on skeletal muscle tone in the conscious rat].

The influence of the skeletal muscle tone by flupirtine (D-9998, Katadolon; CAS 56995-20-1), some selected analgesics and muscle relaxants was investigated in conscious rats after intraperitoneal administration. Benzodiazepines (diazepam and tetrazepam), baclofen, dantrolene and mephenesine reduced the tone of the skeletal muscle. Opiate analgesics, such as morphine, codeine and tramadol, enhanced the muscle tone. Flupirtine reduced the skeletal muscle tone at doses comparable with its antinociceptive effective doses. In this dose range no sedative side effects as ataxia or decrease of spontaneous motor activity could be observed. The mode of this muscle relaxing effect of flupirtine is not known in all details. It is, however, likely that flupirtine is able to inhibit the mono- and/or polysynaptic reflexes at the spinal level.

Aminopyridines↗
PubMedDate not supplied

Effect of a centrally-acting muscle relaxant, eperisone hydrochloride, on muscle sympathetic nerve activity in humans.

The sympatho-modulating effects of eperisone hydrochloride, a centrally acting muscle relaxant, on microneurographically recorded muscle sympathetic nerve activity (MSA) were analyzed in human volunteers. A single dose of 300 mg of eperisone was orally administered to 19 healthy subjects aged between 19 and 27, and effects on 1) spontaneous MSA in 30 degrees head-up tilted position, 2) resting MSA and responsiveness to standing, 3) exercise-induced enhancement of MSA were observed. Eperisone has a sympatho-suppressive action in resting skeletal muscles, but has no effect on MSA in actively contracting muscles, e.g. standing, hand-gripping. The sympatho-suppressive effect of eperisone may be related to the drug-induced increase of blood low in the resting skeletal muscles; also it may be one more mechanism through which the drug can exert its muscle relaxant action.

Adult↗
PubMed1977

A script for deep muscle relaxation.

Deep muscle relaxation has been used as an adjunct to many somatic and psycho-therapies since its introduction by Jacobsen in 1929. It is a therapeutic technique which is taught as a motor skill through the use of instruction, practice, and feedback about progress. The material in this paper provides a script for preparing a relaxation tape for clients to use between or in addition to regular therapy sessions.

Feedback↗
PubMed1990

Recurrent tension headache in adolescents treated with self-help relaxation training and a muscle relaxant drug.

Forty-eight adolescents suffering from recurrent tension headache participated in a controlled trial conducted in a high school setting. During the first treatment phase self-help relaxation training was compared with a waiting-list group. Following this phase a pharmacological regimen consisting of a muscle relaxant (chlormezanone) and placebo was superimposed on relaxation therapy in a double-blind crossover design. Each treatment phase encompassed a 5-week period. In addition to the evaluation of headache complaints, psychological distress among students was measured with respect to their experience of somatic complaints, depressive, anxiety and stress symptoms. Although self-help relaxation training significantly decreased the severity and annoyance of adolescents' headache besides their somatic complaints, the clinical improvement of headache was modest. The addition of chlormezanone did not help those who were nonresponders to self-help relaxation training. Finally, a set of pretreatment variables consisting of baseline headache severity and annoyance, experience of anxiety and daily life stress among adolescents could predict outcome of self-help relaxation therapy.

Adolescent↗
PubMed1991

Abuse of skeletal muscle relaxants.

Centrally acting skeletal muscle relaxants are potential drugs of abuse. Although skeletal muscle relaxants are occasionally the primary drug of abuse, they are often used along with other central nervous system depressants, such as narcotics or alcohol. The major toxic effects are respiratory depression and coma. For the most part, the abuse problem is initiated and sustained iatrogenically. Physicians should be aware of the abuse potential of skeletal muscle relaxants.

Adult↗
PubMedDate not supplied

Some actions of chandonium iodide, a new short-acting muscle relaxant, in anaesthetized cats and on isolated muscle preparations.

1. The actions of the new skeletal muscle relaxant chandonium (HS310) on the cardiovascular, respiratory and skeletal muscle systems of the cat under chloralose anaesthesia and on chick and rat isolated skeletal muscle preparations have been described. 2. In the cat chandonium exhibited a potent, competitive, non-depolarizing neuromuscular blocking action that was rapid in onset and of short duration. It possessed a selective atropine-like action at the cardiac vagus neuro-effector junction but little or no ganglion blocking activity. Neither adrenergic neurone noralpha-adrenoceptor blocking properties were evident. 3. Unlike tubocurarine, chandonium was without effect on the airways system of the anaesthetized cat. 4. Chandonium possessed weak anticholinesterase action. It is conceivable that this effect may contribute to its short duration of action. 5. The results from these studies suggest that chandonium may have possible clinical applications as a short-acting muscle relaxant.

Acetylcholine↗
PubMed1992

[Effects of magnesium and calcium on muscle contractility and neuromuscular blockade produced by muscle relaxants and aminoglycoside].

The muscle contractility and neuromuscular blockade of muscle relaxants are influenced by the electrolytes, especially magnesium ion(Mg2+) and calcium ion(Ca2+), in the extracellular fluid. The present study was designed to evaluate the effects of Mg2+ and Ca2+ on muscle contractility and on the blocking properties of d-tubocurarine, succinylcholine and aminoglycoside antibiotics, tobramycin in vitro, using rats' phrenic nerve-hemidiaphragm preparations. Mg2+ inhibited the twitch tensions in a concentration dependent manner. A low concentration of Ca2+ decreased the twitch tensions, but a high concentration of Ca2+ had no effect on them. Mg2+ potentiated the block produced by d-tubocurarine, succinylcholine and tobramycin depending on the concentration of Mg2+, and good regression lines were obtained. Ca2+, however, antagonized the neuromuscular blockade of the three drugs at any level of Mg2+ concentration. From these findings, it should be noticed that special care must be taken to prevent a profound neuromuscular blockade due to the drug interaction of each drug when a muscle relaxant or an aminoglycoside antibiotics is administered to a patient suffering from hypermagnesemia and/or hypocalcemia.

Aminoglycosides↗
PubMed1975

Antiphosphodiesterase activity and nonspecific smooth muscle relaxation tested on intestinal smooth muscles.

Mitochondrial, microsomal and soluble fractions separated from the guinea pig taenia and from the dog longitudinal smooth muscle were used as phosphodiesterase preparation. Each preparation had low and high Km values, indicating the existence of at least two kinds of phosphodiesterase. Papaverine and Aspaminol (1, 1-diphenyl-3-piperidinobutanol hydrochloride), hydralazine, caffeine Na benzoate and aminophylline were used at test drugs. Aspaminol had little inhibitory effect on phosphodiesterase. Ki value of papaverine almost equalled the concentration (M) which was necessary to produce 50% relaxation. Relaxation of the guinea pig taenia by papaverine was preceded by an increase of intracellular cyclic AMP,. Therefore, the action of papaverine is likely to be mediated by an increase in cyclic AMP, which is caused by inhibition of the phosphodiesterase-catalyzed breakdown of cyclic AMP. There was little correlation between relaxing activities of the drugs used and their antiphosphodiesterase activities. Relaxation of the smooth muscle induced by the smooth muscle relaxants excepting papaverine is not due to inhibition of phosphodiesterase.

Animals↗
PubMedDate not supplied

Prolonged myasthenic syndrome after one week of muscle relaxants.

A child developed severe, generalized muscle weakness which persisted for 6 weeks, after receiving muscle relaxants for 1 week while requiring ventilator support. Electrodiagnostic studies indicated a presynaptic disorder of the neuromuscular junction which improved with high-frequency stimulation, similar to findings in Lambert-Eaton syndrome. Muscle specimens exhibited neurogenic targetoid fiber atrophy. Ultrastructure of the neuromuscular junction indicated terminal axon degeneration and atrophy with depletion of the secretory vesicles. Most reported patients with post-ventilator paresis have received steroids and muscle relaxants; muscle weakness commonly has been brief and attributed to steroids. We believe that this reversible myasthenic syndrome probably represents neurotoxicity due to high doses of steroidal nondepolarizing blocking agents; however, available data are insufficient to resolve this controversy.

Atrophy↗
PubMed1990

Substantia nigra: a site of action of muscle relaxant drugs.

Sites of action of centrally active muscle relaxant drugs are not well defined. Clinical experience with such drugs suggests that the spinal cord may be one of the important regions from which pathologically increased muscle tone may be relieved. Supraspinal centers that may also be involved in the expression of muscle relaxant action have not yet been defined. We report here that microinjections of therapeutically relevant muscle relaxants into the midbrain tegmentum of genetically spastic rats decrease muscle tone. The substantia nigra is the region from which midazolam, baclofen, and tizanidine (drugs used clinically in the treatment of spasticity), or gamma-vinyl-GABA, (-)-2-amino-7-phosphonoheptanoate, and [D-pro2-D-phe7-D-trp9]-substance P (experimental drugs active in animal models of spasticity), reduce muscle tone in genetically spastic rats and Hoffmann reflexes in normal rats. The effects of muscle relaxant drugs are topographically restricted to the substantia nigra pars reticulata and are receptor specific. These observations disclose a previously unknown function of the substantia nigra in mediating muscle relaxation.

Animals↗
PubMed1992

Iontophoretic study of speed of action of various muscle relaxants.

The speed of action of nondepolarizing muscle relaxants is inversely related to potency. The hypothesis that this effect occurs at the end plate was tested in a frog (Rana pipiens) cutaneous pectoris muscle preparation. Brief acetylcholine pulses (10-100 ms) were applied iontophoretically from a central barrel of a triple-barrelled microelectrode located near an end plate. Long pulses (10-200 s) of muscle relaxant (gallamine, rocuronium, d-tubocurarine, atracurium, vecuronium, pancuronium, and doxacurium) were applied from one of two other barrels. The responses were a voltage change at the end plate, measured with an intracellular electrode. To evaluate potency, intracellular voltage changes following iontophoretic acetylcholine pulses were measured after application of various concentrations of muscle relaxants. The following were the equilibrium dissociation constants, which represent concentration of relaxant for 50% inhibition of response (mean plus or minus standard deviation): gallamine, 4.56 +/- 0.44 microM (n = 5); rocuronium, 0.71 +/- 0.09 microM (n = 6); d-tubocurarine, 0.59 +/- 0.07 microM (n = 4); atracurium, 0.31 +/- 0.03 microM (n = 4); vecuronium, 0.23 +/- 0.02 microM (n = 5); pancuronium, 0.18 +/- 0.03 microM (n = 3); doxacurium, 0.11 +/- 0.03 microM (n = 5). Both onset and offset of effect of muscle relaxant proceeded with an exponential time course.(ABSTRACT TRUNCATED AT 250 WORDS)

Androstanols↗