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At least 37 records · Page 2Linked to original sources
PubMed1979

Behavioral intervention with muscle-contraction headache: a review.

Studies involving behavioral intervention with muscle-contraction headache are reviewed. Intervention approaches have most frequently involved frontal electromyographic feedback and relaxation instructions. Although behavioral intervention packages have been more effective than control procedures in reducing headache activity, identification of active components of these packages is difficult. Specifically,, the contribution of placebo, expectancy and demand factors, reactive effects of self-monitoring, and home practice have not been adequately assessed. The importance of assessing individual differences in etiology and in response to intervention is stressed. The results of some studies are congruent with the hypothesized muscle tension etiology of muscle-contraction headaches but the results from others suggest that factors other than muscle-tension may be involved. Supportive laboratory research on the intervention procedures and cost-efficiency of electromyographic feedback and relaxation instructions are discussed.

Attitude↗
PubMed1979

Controlled trial of EMG feedback in muscle contraction headache.

Twenty-eight patients suffering from severe, longstanding muscle contraction headache were randomly assigned to two groups, one receiving electromyographic (EMG) feedback therapy and the other, "most suitable alternative therapy." Headache intensity and severity as well as drug intake were reduced in the feedback group (p less than or equal to 0.01) as opposed to no improvement in the control group. The positive treatment effect in the feedback group persisted through a three-month follow-up period. EMG feedback therapy is effective in the treatment of muscle contraction headache even in its chronic, severe form, which is resistant to traditional treatment methods.

Adult↗
PubMed1979

Inhibition of intestinal smooth muscle contraction by surface-active alkyltrimethylammonium salts.

The effects of surface-active alkyltrimethylammonium salts (C10--C20) on the contractile activity of isolated rat jejunum and on the gastrointestinal motility in anaesthetized rats were studied. The surfactants caused a dose-dependent depression of spontaneous contractions and of acetyl-beta-methylcholine and BaCl2 induced contractions of isolated rat jejunum. The depressant activity of the surface-active alkyltrimethylammonium salts on smooth muscle contraction increased with an increase in the length of the alkyl chain to maximum activity at C16. It is suggested that the depressant activity of the surface-active alkyltrimethylammonium salts on smooth muscle contraction is due to a non-specific interaction of the surfactants with the cellmembrane of the muscle cells. No effect on gastric and intestinal motility in vivo was observed following intragastric or intraintestinal administrations of surface-active alkyltrimethylammonium salts. This lack of effect upon intraintestinal or intragastric administration probably depends on an inability of the surfactants to reach the site of action when administered from the mucosal side.

Acetylcholine↗
PubMed1976

Myotonia congenita with painful muscle contractions.

We present a family with dominantly inherited myotonia congenita and painful, electrically silent muscle contractions after exertion. In two family members, painful muscle contractions occurred coincident with hypothyroidism, and improved after thyroid replacement therapy. It is probable that this family represents a disease that is similar to but distinct from the dominant form of myotonia congenita.

Adult↗
PubMed1978

Correlation between the effects of salbutamol on contractions and cyclic AMP content of isolated fast-and slow-contracting muscles of the guinea pig.

The effects of isoprenaline and salbutamol on incomplete tetanic contractions of the isolated soleus (slow contracting) and extensor digitorum longus (EDL-fast-contracting) muscles of the guinea pig were studied and an attempt made to correlate these effects on contractility with changes in cyclic AMP concentrations. Salbutamol was 10-12 times less potent than (+/-)isoprenaline in decreasing the force of subtetanic contractions in the soleus and between 5-6 times less potent in increasing the force of subtetanic contractions in the EDL. This observation plus the lack of activity of both the selective beta1-adrenoceptor antagonist (atenolol) and the selective beta1 agonist (H 133/22) in the EDL implies involvement of beta2-adrenoceptors in these responses of the muscles to isoprenaline and salbutamol. The soleus muscle was about 6-12 times more sensitive to effects of beta-adrenoceptor agonists than the EDL. In concentrations which produced effects on muscle contractility, salbutamol significantly elevated cyclic AMP concentrations in both types of muscle. These effects were antagonised by propranolol. It seems clear that the contrasting effects of sympathomimetic amines on slow-and fast contracting muscle are mediated through a common mechanism-elevation of cyclic AMP. Possible explanations of this apparent paradox are discussed.

Albuterol↗
PubMed1977

Equatorial x-ray reflections from contracting muscle after an applied stretch.

The equatorial X-ray reflections were recorded from contracting muscle after a slow stretch. The intensity ratio of the 1,0 to the 1,1 reflections (I10/I11) after the stretch was not significantly different from that during an isometric tetanus at the same sarcomere length, although the tension after the stretch was considerably greater than isometric. This suggests that an almost identical number of cross-bridges produce a greater tension after a slow stretch than during an isometric tetanus.

Animals↗
PubMedDate not supplied

[Effect of sydnophen and caffeine on reflex shifts in arterial pressure arising during skeletal muscle contraction].

The influence of sydnophen (5-20 mg/kg) and of caffein (10-40 mg/kg) on the pressor reaction of the arterial pressure, provoked by contraction of skeletal muscles following stimulation of the anterior spinal cord roots (L6, L7, S1) was investigated in 17 tests set up on decerebrated non-narcotized cats. The intraveonus injection of sydnophen was attended by a fall of the arterial pressure and inhibition of the pressor reflex. Caffein reduced the intensity of the pressor reflex to a lesser extent and did not modify the initial level of the arterial pressure.

Animals↗
PubMed2026

Signaling mechanisms of vasopressin/oxytocin-type neuropeptide-induced muscle contraction in the sea cucumber Apostichopus japonicus.

The myoregulatory action of vasopressin/oxytocin (VP/OT)-type neuropeptides is evolutionarily conserved across Bilateria. In vertebrates, the signaling cascades involved have been comprehensively characterized in several muscle types, including uterine and gastrointestinal smooth muscles. VP/OT-type neuropeptide-induced muscle contraction or relaxation has been reported in a variety of invertebrates, but the downstream signaling pathways responsible for these effects have yet to be elucidated. Here, using heterologous cell systems and in vitro pharmacological experiments, we investigated the signaling pathways underlying VP/OT-type neuropeptide (holotocin) induced contraction of the longitudinal muscle of the body wall (LMBW) in the sea cucumber Apostichopus japonicus (phylum Echinodermata), a deuterostome invertebrate. Holotocin-induced contraction of the LMBW comprised two distinct phases: an initial rapid phasic contraction followed by a sustained tonic contraction. Pharmacological experiments revealed that upon binding to its receptor AjHOR, holotocin activates a Gαq-dependent pathway, leading to phospholipase C (PLC) activation and subsequent hydrolysis of phosphatidylinositol 4,5-bisphosphate (PIP2) into inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). IP3 triggers Ca2+ release from intracellular Ca2+ stores via IP₃ receptors (IP3R), but depletion of intracellular Ca2+ does not activate store-operated Ca2+ entry (SOCE). DAG activates protein kinase C (PKC), which may modulate the activity of ion channels in the plasma membrane, resulting in membrane depolarization, opening of voltage-gated Ca2+ channels (VGCCs), and subsequent influx of extracellular Ca2+. Overall, this study reveals similarities and differences in the signaling pathways mediating smooth muscle contraction in invertebrates and vertebrates, providing new insights into the evolution of these mechanisms across the Bilateria.

Ca(2+)↗
PubMed1978

Changes in the kinetics of muscle contraction in vitamin D-depleted rats.

Using an in situ rat soleus neuromuscular preparation, changes in the muscle contraction kinetics in response to vitamine D depletion were studied. For a single isometric contraction, the time-to-peak tension (Tp) and the time-for-recovery-half-way-to-resting tension (T1/2r) were recorded. For a 150 Hz, 300 msec tetanus, the T1/2r was determined. Animals raised on high-calcium, high-phosphate, vitamin D-depleted diets showed prolongation of all parameters. Repletion of vitamin D returned Tp and T1/2r values to normal. Neither dietary calcium deficiency nor thyroparathyroidectomy produced an prolongation of Tp or T1/2r values. Therefore, based upon the experimental data, it appears that vitamin D or one of its metabolites, independent of any effect on the serum calcium or serum phosphate concentration, is necessary for normal muscle relaxation.

Animals↗
PubMedDate not supplied

[Membrane mechanisms of activating depolarized smooth muscle contraction (guinea pig small intestine) during exposure to physiologically active compounds].

The experiments were performed on the depolarized smooth muscle of taenia coli with the use of double sucrose-gap arrangement. Muscle contractions were induced by 1) application of hystamin or bradikynin; 2) rectangular long-lasting (10--20 s) pulses of hyperpolarizing current--the strong contraction appeared in response to the switching off the current (off-response). Both the on- and off-responses to the hyperpolarizing current recorded before, during and after hystamine (or bradikynin)-induced contration were, as a rule, very similar. Treatment of smooth muscle with local anaesthetics (procaine, trimecaine, QX-572) removed hystamine- and bradikynin-induced contrations and only decreased off-responses. The analysis of the data obtained suggested the existence of the independent electrically and chemically excitable systems (channels?) OF Ca2+ ion transport in the membrane of smooth muscle cells.

Animals↗
PubMed1978

Modification of combined migraine-muscle contraction headaches using BVP and EMG feedback.

The effect of blood volume pulse (BVP) and frontalis muscle action potential (EMG) feedback on control of vasoconstriction of the temporal artery and frontalis muscle activity in combined migraine-muscle tension subjects was investigated in a multiple baseline design (across subjects and responses). The data indicated: (a) both subjects obtained an ability to control BVP during BVP feedback and EMG during EMG feedback; (b) there were decreases in frequency of migraine headaches during BVP feedback and decreases in muscle contraction headaches during EMG feedback. The results of this study supported the theoretical explanation of two pain mechanisms involved in combined muscle contraction-migraine headaches as well as the effectiveness of bio-feedback procedures that target directly the specific pain mechanism in the elimination of the two types of head pain.

Adult↗
PubMed1977

Return of myosin heads to thick filaments after muscle contraction.

The heads of myosin molecules, which move to the vicinity of the thin filaments to react with actin during muscle contraction, return to the thick filaments after contraction. The return occurs in two stages; a rapid return of the majority of the myosin heads is followed by a slow return of the rest.

Animals↗
PubMed1978

Neostigmine-induced alterations at the mammalian neuromuscular junction. I. Muscle contraction and electrophysiology.

The effects of single and repetitive injections of neostigmine on neuromuscular physiology were examined in rat extensor digitorum longus muscles. The characteristic facilitation of neuromuscular transmission associated with acute anticholinesterase treatment was accompanied by significant pre- and postsynaptic alterations in neuromuscular transmission. Three days of neostigmine treatment caused a decrease in indirectly and directly elicited muscle contraction. Miniature end-plate potential amplitude and frequency, end-plate potential amplitude, junctional acetylcholine sensitivity and quantal content of nerve-evoked end-plate potentials were also decreased by this treatment. By 22 to 25 days of continued treatment, the decreased rate of transmitter release had returned almost to normal, whereas the alterations of the postsynaptic membrane persisted for as long as 106 days. Alterations were also found in the muscle action potential and in certain passive electrical properties of the extrajunctional muscle membrane. In addition, many of the physiological changes were correlated directly with the morphological changes observed in rats treated similarly. We conclude that neostigmine treatment in rats in therapeutic doses has deleterious effects on neuromuscular physiology and neuromuscular ultrastructure. Although the pattern of these changes is not identical with that seen in rabbit and human myasthenia gravis, the neostigmine treatment used in patients with myasthenia gravis may contribute in part to the neuromuscular alterations observed in this disease.

Acetylcholine↗
PubMedDate not supplied

Prevention of persistent cerebral smooth muscle contraction in response to whole blood.

Using an in vitro system designed to measure arterial constriction, we have demonstrated the importance of platelet function in maintaining cerebral smooth muscle contraction after whole blood injection. We tested two agents, acetyl salicylic acid (ASA) and phthalazinol, both known to interfere with platelet function. In control tests normal rabbit and monkey blood produced a reliable and persistent arterial constriction. In experimental tests blood drawn from animals premedicated with ASA and phthalazinol failed to produce a persistent contraction. These results support the hypothesis that chemicals released during platelet aggregation may be important in persistent vasospasm.

Animals↗
PubMedDate not supplied

[Molecular mechanism of muscle contraction: the straightening of the bent actomyosin bond].

A new molecular mechanism of muscle contraction is considered based on the cyclochelate oxyphosphorane structure of the long-lived intermediate in myosin-catalyzed ATP. Mg hydrolysis proposed earlier by the author. The mechanism implies the steric cleavage of the actomyosin bond by the gamma-phosphoryl group of ATP.Mg tightly binding to myosin; the myosin-catalyzed addition of water to the gamma-phosphoryl group to give oxyphosphorane group which sterically allows the formation of a more weak bent (deformed) actomyosin bond; the actin-catalyzed breakdown of the tightly bound oxyphosphorane intermediate into weakly bound products; the straightening of the bent actomyosin bond with the active change of an angle of myosin head attachment, the liberation of the weakly bound products and the displacement of the actin filament. The data are given in favour of an oxyphosphorane structure of the long-lived intermediate.

Actomyosin↗