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At least 379 records · Page 21Linked to original sources

PubMed1984

Detection of stimulated back muscle contractions by moiré topography.

The ability to treat scoliosis via surface stimulated trunk muscle contractions is now being evaluated at several treatment centers. In order to make biomechanical analysis of the procedure, so that the technique can be used optimally, data are needed to quantify the muscle contractions and structural changes by different electrode locations. This paper presents the use of a modified shadow moiré technique to quantify geometric changes resulting from electrical stimulation applied to the surface of the back in a healthy subject.

Back↗

PubMed2004

Time series analysis of jaw muscle contraction and tissue deformation during mastication in miniature pigs.

Masticatory muscle contraction causes both jaw movement and tissue deformation during function. Natural chewing data from 25 adult miniature pigs were studied by means of time series analysis. The data set included simultaneous recordings of electromyography (EMG) from bilateral masseter (MA), zygomaticomandibularis (ZM) and lateral pterygoid muscles, bone surface strains from the left squamosal bone (SQ), condylar neck (CD) and mandibular corpus (MD), and linear deformation of the capsule of the jaw joint measured bilaterally using differential variable reluctance transducers. Pairwise comparisons were examined by calculating the cross-correlation functions. Jaw-adductor muscle activity of MA and ZM was found to be highly cross-correlated with CD and SQ strains and weakly with MD strain. No muscle's activity was strongly linked to capsular deformation of the jaw joint, nor were bone strains and capsular deformation tightly linked. Homologous muscle pairs showed the greatest synchronization of signals, but the signals themselves were not significantly more correlated than those of non-homologous muscle pairs. These results suggested that bone strains and capsular deformation are driven by different mechanical regimes. Muscle contraction and ensuing reaction forces are probably responsible for bone strains, whereas capsular deformation is more likely a product of movement.

Animals↗

PubMed1980

Cross-bridge model of muscle contraction. Quantitative analysis.

We recently presented, in a qualitative manner, a cross-bridge model of muscle contraction which was based on a biochemical kinetic cycle for the actomyosin ATPase activity. This cross-bridge model consisted of two cross-bridge states detached from actin and two cross-bridge states attached to actin. In the present paper, we attempt to fit this model quantitatively to both biochemical and physiological data. We find that the resulting complete cross-bridge model is able to account reasonably well for both the isometric transient data observed when a muscle is subjected to a sudden change in length and for the relationship between the velocity of muscle contraction in vivo and the actomyosin ATPase activity in vitro. This model also illustrates the interrelationship between biochemical and physiological data necessary for the development of a complete cross-bridge model of muscle contraction.

Actins↗

PubMed1989

Effects of cromakalim on acetylcholine release and smooth muscle contraction in guinea-pig small intestine.

The effects of the potassium channel opener cromakalim on smooth muscle contraction and 3H-acetyl-choline release were studied simultaneously in guinea-pig longitudinal muscle myenteric plexus preparations which had been preincubated with 3H-choline. Cromakalim (10 mumol/l) inhibited more markedly the smooth muscle contractions caused by the release of endogenous acetylcholine (via electrical stimulation or via activation of nicotine- and 5-HT3-receptors) than contractions induced by pilocarpine. Cromakalim (10 mumol/l) did not affect the release of 3H-acetylcholine evoked by electrical stimulation or by stimulation of nicotine- and 5-HT3-receptors. In contrast, the release of 3H-acetylcholine caused by stimulation of M1-receptors was concentration-dependently reduced by cromakalim (1-100 mumol/l). The results suggest that the relaxant effect of cromakalim on smooth muscle contraction is not caused by a reduction of acetylcholine release from myenteric neurones. An opening of cromakalim-sensitive potassium channels may be involved in the inhibition of the M1-receptor mediated acetylcholine release.

Acetylcholine↗

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↗

PubMed2005

The simultaneous collapse of both the swinging crossbridge theory of muscle contraction and the in vitro motility essays.

In the early seventies we discovered that isolated, active, myosin fragments can induce movement and tension generation by actin filaments in both in vitro and in vivo systems, employing a variety of techniques. It was not in line with the domineering swinging crossbridge theory of muscle contraction. We then proposed an hydrodynamic mechanism which explained our results and was applied to muscle contraction and to other biological engines. Our discovery has been ignored for a long time until the so-called "in vitro motility essays" appeared. By using this artifact--laden technique the mechanochemical reactivity of the active myosin fragments was re-discovered without giving us any credit. The essays gave continuously changing values for fundamental parameters of muscle contraction; the values were appreciably different in different laboratories and decreased in a continuous fashion in the hands of one scientist. By analyzing recent experiments which derived the rate of ATP hydrolysis of active muscles as function of the applied load I calculated the value of the sliding distance resulting from the breakdown of one ATP molecule by each of the myosin heads in contracting muscle. According to the contemporary theory this should be the same for all muscles under any environmental conditions and determined by length of the myosin head's neck. My examination led to the conclusion that the sliding distance varies from one muscle to another and with different temperatures for the same muscle. This again, contradicts the current theory and should give the final blow to both this theory and the "essays". Furthermore: it can be explained by a hydrodynamic mechanism such as that proposed by us more than 30 years ago.

Actin Cytoskeleton↗

PubMed1993

Inhibitory effects of four inhaled anesthetics on canine tracheal smooth muscle contraction and intracellular Ca2+ concentration.

To clarify the mechanisms by which inhaled anesthetics directly inhibit tracheal smooth muscle contraction, we investigated the effects of these anesthetics on muscle tension and intracellular Ca2+ concentration ([Ca2+]i). Tension was measured using an isometric transducer, and [Ca2+]i was measured using Fura-2, an indicator of [Ca2+]i. Addition of 1 microM carbachol increased muscle tension and [Ca2+]i. All inhaled anesthetics significantly decreased both muscle tension and [Ca2+]i in the following order of inhibitory potency: halothane >> isoflurane > enflurane >> sevoflurane. In the presence of 10 microM verapamil, carbachol moderately increased muscle tension, but induced a transient increase of [Ca2+]i followed by a substantial reduction. Inhaled anesthetics in the presence of both carbachol and verapamil significantly decreased muscle tension without decreasing [Ca2+]i. Potency for suppression of tension under these conditions, which appeared to be independent of [Ca2+]i, was in the order: halothane >> enflurane > or = isoflurane >> sevoflurane. The best correlation we found with a measured reduction of muscle tension independent of [Ca2+]i was with oil/gas partition coefficients (r = -0.88, P < 0.001). In conclusion, inhaled anesthetics inhibit tracheal smooth muscle contraction by at least two mechanisms: 1) reduction of [Ca2+]i and 2) suppression of contractility, independent of [Ca2+]i. The close correlation between the muscle inhibition independent of [Ca2+]i and the oil/gas partition coefficients suggests that one of the major sites of action of inhaled anesthetics is membrane phospholipids.

Anesthetics↗

PubMed2000

Endomorphin-1 and -2, endogenous ligands for the mu-opioid receptor, inhibit striated and smooth muscle contraction in the rat oesophagus.

Recently, morphological evidence for an interaction of autonomic nerve fibres and extrinsic motor innervation of the rat oesophagus has emerged. The aim of the present study was to investigate the possible influence of endogenous and exogenous opioids on rat oesophageal smooth and striated muscle function in vitro. The entire oesophagus (excluding the lower oesophageal sphincter) with both Nervi (Nn) vagi, including the Nn recurrentes, was dissected and placed in an organ bath (100 mL, 37 degrees) with oxygenated Krebs-Ringer buffer. Contractile activity was measured in a longitudinal direction with a force transducer. Both Nn vagi were placed on a bipolar platinum electrode 2 cm distant from the oesophagus. Vagal stimulation (VS), applied for 1 s (40 V, 0.5 ms, 20 Hz) resulted in a biphasic contractile response that was completely blocked by 10(-6) M tetrodotoxin. The first part consisted of a tetanic striated muscle contraction, as it was abolished by tubocurarine (10(-5) M, n=5) but unaffected by atropine (10(-6) M, n=3) or hexamethonium (10(-4) M, n=4). In contrast, the second part was completely inhibited by hexamethonium (10(-4) M) and atropine (10(-6)M), whereas tubocurarine (10(-5) M) showed no influence, indicating a stimulation of preganglionic nerve fibres supplying oesophageal smooth muscle (muscularis mucosae) via relays in myenteric ganglia. In order to characterize opioid influence on the oesophageal striated and smooth muscle contractility, the following experiments were carried out. 10(-6) M endomorphin-1 and -2, endogenous mu-opioid-receptor agonists, reduced the contractile response of the striated (EM-2, -25.1+/-5.3%; n=16), and the smooth muscle (EM-2, -81.9+/-3.3%; n=11). Both effects were reversible by the opioid receptor antagonist naloxone (10(-6) M) and therefore, mediated via opioid receptors. Neither SNC-80, an agonist on the delta-opioid-receptor, U-69593, an agonist on the kappa-opioid-receptor, nor nociceptin, an agonist at the ORL1 (opioid receptor-like) receptor, had a significant effect on the striated muscle contraction. In contrast to SNC-80, U-69593 and nociceptin inhibited smooth muscle contraction but this relaxation could not be antagonized by naloxone. None of the opioid receptor antagonists used had an effect on basal tonus or muscle contraction following VS. Our data provide evidence for an autonomic modulation of vagal motor innervation of the striated and smooth oesophageal muscle. Endomorphin-1 and -2, both selective mu-opioid receptor agonists, cause an inhibition of striated and smooth muscle response which is reversible by naloxone, an opioid receptor antagonist. The location of the mu-opioid receptor still has to be established.

Animals↗

PubMed2006

Rho-kinase-mediated regulation of receptor-agonist-stimulated smooth muscle contraction.

Rho kinase was shown to regulate smooth muscle contraction through modulating myosin phosphatase (MLCP) activity, but the in vivo mechanism remains to be clarified. This study examined the effects of Rho kinase inhibition on the phosphorylation time course of MLCP subunit MYPT1 at Thr697 and Thr855 and MLCP inhibitory protein CPI-17 at Thr38 and on actin polymerization during the contraction of rat tail artery (RTA) smooth muscle. Rho kinase inhibitor Y27632 suppressed force activated by alpha(1)-adrenergic agonist phenylephrine or thromboxane A(2) analog U46619 with concomitant decreases in MLC(20) phosphorylation. Phenylephrine and U46619 significantly increased MYPT1(Thr855) phosphorylation that was eliminated by Y27632 pretreatment, whereas MYPT1(Thr697) phosphorylation was not stimulated. Phenylephrine increased CPI-17(Thr38) phosphorylation that was not inhibited by Y27632 but was abolished by a protein kinase C inhibitor Ro 31-8220; in contrast, U46619 did not stimulate CPI-17 phosphorylation. Both agonists increased actin polymerization that was diminished by Y27632 under phenylephrine but not U46619 activation. These results demonstrated a temporal correlation between MYPT1(Thr855) phosphorylation, MLC(20) phosphorylation, and contraction in a Rho-kinase-dependent manner for both phenylephrine and U46619 stimulation, suggesting that Rho kinase regulates MLCP activity through MYPT1(Thr855) phosphorylation during RTA smooth muscle contraction. Furthermore, Rho kinase regulates actin polymerization activated by alpha(1)-adrenoceptors but is less significant in thromboxane receptor stimulation.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed2005

The role of sphingosine-1-phosphate in smooth muscle contraction.

Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid metabolite that is known to mediate diverse cellular responses including cell growth, survival, and migration. Most of these effects have been attributed to its binding to a specific subfamily of G protein-coupled receptors (GPCR), namely S1P(1-5). Recent studies have suggested that S1P also plays a prominent role in the contraction of various types of smooth muscle. This review provides a brief overview of its role in this process and also highlights how S1P-dependent signaling serves as an important regulator of smooth muscle contraction.

Animals↗

PubMed1997

Forelimb muscle contraction induced by cerebral cortical stimulation after callosotomy: a myographic study in the mouse.

The effect of callosotomy upon motor control by the cerebral cortex on the forelimb was examined in the mouse. On the 10th day after callosotomy in the rostral or caudal part of the corpus callosum, the forelimb area of the cerebral motor cortex was stimulated intracortically with a microelectrode and muscle contraction of the forelimb was recorded by electromyography. Muscle contraction was observed in the contralateral forelimb in the mice of which callosal fibers were cut in the caudal part of the corpus callosum including the splenium corporis callosi as well as in the normal mice. On the other hand, muscle contraction was observed in the ipsilateral forelimb in the mice of which callosal fibers were incised in the rostral part of the corpus callosum including the genu, rostrum and trunk. The latency of the muscle contraction was about 0.5 msec in the both groups of the callosotomized mice, as well as in the normal mice.

Animals↗

PubMed1988

The function of two heads of myosin in muscle contraction.

Myosin has two heads which can bind with F-actin and react with ATP. The skeletal muscle myosin forms each 1 mol of the myosin-phosphate-ADP complex (M-P-ADP) and the myosin-ATP complex (M-ATP). The actomyosin ATPase reaction which is coupled with muscle contraction is catalyzed only by the head which forms M-P-ADP. However, the function of M-ATP forming head in muscle contraction has not been elucidated. We studied the binding of S-1 and HMM with F-actin and the dissociation of acto-S-1 or acto-HMM by ATP or AMPPNP using the change in light-scattering and fluorescence of pyrene bound to F-actin. S-1 and HMM bound with actin at 1:1 and 1:2 molar ratio, respectively. Acto-S-1 dissociated by one mole of ATP per mole of S-1 but acto-HMM dissociated by 1 mol ATP per mol of HMM (0.5 mol/mol head). Acto-HMM dissociates by AMPPNP (or ADP) via a ternally complex. Acto-HMM bound two mole of AMPPNP, but acto-HMM dissociated by a function of (AMPPNP) but not (AMPPNP)2. These results suggested that the affinity of HMM with F-actin decreased by the binding of one mole of AMPPNP. The result presented here showed that binding of M-ATP forming head with F-actin is controlled by the ATPase reaction of the M-P-ADP forming head. It is suggested that during muscle contraction two heads react cooperatively with thin filament.

Actins↗

PubMed2003

Airway smooth muscle: contraction and beyond.

Airway smooth muscle (ASM), an important tissue involved in the regulation of bronchomotor tone, exists in the trachea and in the bronchial tree up to the terminal bronchioles. The physiological relevance of ASM in healthy airways remains unclear. Evidence, however, suggests that ASM undergoes marked phenotypic modulation in lung development and in disease states such as asthma, chronic bronchitis and emphysema. The shortening of ASM regulates airway luminal diameter and modulates airway resistance, which can be augmented by cytokines as well as extracellular matrix alterations. ASM may also serve immunomodulatory functions, which are mediated by the secretion of pro-inflammatory mediators such as cytokines and chemokines. In addition, ASM mass increases in chronic airway diseases and may represent either a pathologic or an injury-repair response due to chronic inflammation. This review will present evidence that ASM, a "passive" contractile tissue, may become an "active participant" in modulating inflammation in chronic lung diseases. Cell facts 1. Found in the trachea and along the bronchial tree. 2. Critically important in regulating bronchomotor tone of the airways. 3. Differentiation state is associated with the expression of various "contractile proteins." 4. Displays phenotypic modulation of mechanical, synthetic and proliferative responses. 5. Secretes cytokines, chemokines and extracellular matrix proteins. 6. May serve as a potential new target for the treatment of chronic lung diseases.

Animals↗

PubMed1990

Headache versus nonheadache state: a study of electrophysiological and affective changes during muscle contraction headaches.

Seventeen carefully screened muscle contraction headache sufferers were tested in both the headache and the nonheadache state. At baseline, forehead and trapezius EMG were higher, whereas finger temperature and finger blood volume were lower in the headache than the nonheadache state. At a borderline level, physiological reactivity was greater during the headache than the nonheadache state in response to a reaction-time stressor. During the headache state, subjects also reported themselves to be more anxious, depressed, and angry than they were in the nonheadache state and said they felt themselves to be more hassled by external stressors and less able to cope with, prevent, and control their headaches. The findings are consistent with the notion that shoulder/neck tension and emotional arousal contribute to tension headaches. Evidence is less clear for the contribution of vasomotor factors and general physiological reactivity.

Adult↗

PubMed1999

Professor Ebashi's impact on the study of the regulation of striated muscle contraction.

The field of striated muscle regulation has changed tremendously over the last forty years. Many of the problems solved by Dr. Ebashi and by those stimulated by him offer new challenges for future generations of scientists. Many questions remain to be solved, and it should give particular pleasure to Dr. Ebashi to see how the seeds sown by him and his colleagues have now grown into a beautiful tree that bears rich fruit at present and will continue to do so for a long time in the future.

Actins↗

PubMed2005

Calcineurin regulates enteric muscle contraction through EXP-1, excitatory GABA-gated channel, in C. elegans.

The enteric muscle contraction (EMC) is the last step of the defecation behavior which occurs every 50 s in Caenorhabditis elegans. This EMC is regulated by intestinal and anal depressor muscles, which are innervated by GABA motor neurons. Our data show that calcineurin (tax-6) is expressed in intestinal muscle and anal depressor muscle, and the gain-of-function mutant of calcineurin, tax-6(jh107), shows defects in enteric muscle contractions. In addition, the intracellular region of EXP-1, an excitatory GABA receptor, specifically binds to calcineurin A. This interaction between TAX-6 and EXP-1 appears to be independent of both calcium and CNB, which is the calcium-binding regulatory subunit. Genetic evidence of epistasis between cnb-1(jh103) and exp-1(sa6) suggests that calcineurin functions as a negative regulator of excitatory GABA receptor in GABA signaling in C.elegans.

Amino Acid Sequence↗

PubMed2001

S100A1 modulates skeletal muscle contraction by desensitizing calcium activation of isometric tension, stiffness and ATPase.

S100, a subfamily of the EF-hand type calcium sensing proteins, is implicated in many cellular functions including muscle contractility. Two isoforms, S100A1 and S100B, at 2-10 microM significantly inhibit active tension, stiffness and ATPase of skinned single rabbit psoas muscle fibers at sub-maximal (pCa approximately 6.1-5.6), but not at maximal levels of activation (pCa 4.0). S100A1 is a more potent inhibitor than S100B. Hill analysis of the ATPase-pCa and tension-pCa curves indicates that these proteins reduce calcium sensitivity and enhance the cooperativity toward calcium. We propose S100A1, and perhaps S100B, are viable candidates as physiological modulators of muscle contraction.

Adenosine Triphosphatases↗

PubMed2003

Chronic ischemia increases prostatic smooth muscle contraction in the rabbit.

PURPOSE: We studied the effect of chronic ischemia on prostatic smooth muscle contraction in the rabbit. MATERIALS AND METHODS: New Zealand male rabbits weighing 3 to 3.5 kg were assigned to 2 groups. Group 1 (10 rabbits) underwent balloon endothelial injury of the iliac arteries and received a 0.5% cholesterol diet for 4 weeks and then a regular diet for 8 weeks. Control group 2 (10 rabbits) received a regular diet. After 12 weeks the animals were anesthetized. Iliac artery and prostate blood flow was recorded. Prostate tissues were prepared for isometric tension measurement, enzyme immunoassay to determine cyclic guanosine monophosphate (cGMP) release and histological examination. RESULTS: In group 1 atherosclerosis as well as a significant decrease in iliac artery and prostate blood flow were observed. Ischemia significantly increased prostatic tissue contraction, decreased cGMP release and led to capsular and stromal thickening, and epithelial atrophy. The alpha1-adrenoceptor blocker doxazosin and the phosphodiesterase-5 inhibitor sildenafil citrate significantly decreased the contraction of control and ischemic tissues. Doxazosin was more effective in decreasing contractions when it was combined with sildenafil or the nitric oxide (NO) precursor L-arginine. In contrast, doxazosin was less effective when it was combined with the NO synthase inhibitor N omega-nitro-L-arginine or with the guanylate cyclase inhibitor methylene blue. Doxazosin significantly increased cGMP release in control tissues but not in ischemic tissues. Sildenafil significantly increased cGMP release in control and ischemic tissues. CONCLUSIONS: Ischemia increased prostatic smooth muscle contraction and led to marked structural damage. Stimulators of NO synthesis and cGMP production enhanced the efficacy of doxazosin in decreasing prostatic tissue contraction. Sildenafil decreased contractility and increased cGMP release. Increased smooth muscle tone and structural changes in the ischemic prostate may suggest a role for prostate ischemia in resistance to urinary flow independent of prostate size.

Adrenergic alpha-Antagonists↗