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At least 829 records · Page 46Linked to original sources

PubMed1979

Combination bronchodilators: antagonism of airway smooth muscle contractions in vitro.

The component drugs of fixed-dose combination bronchodilators may interact in a synergistic manner to antagonize airway contractions. To examine this hypothesis, combinations of ephedrine (E) and theophylline (Th) or salbutamol (S) and theophylline were tested for their ability to relax contracted guinea-pig airway smooth muscle in vitro. The combination bronchodilator effect was compared to the summed effects of the component drugs given individually (i.e. a theoretical additive response, Ta). Relaxation responses to combination bronchodilators were considered less-than-additive if significantly less than Ta, additive if non-significant and greater-than-additive or synergistic if the values were significantly greater than Ta. It was found that the E-Th combinations interacted primarily in an additive fashion to relax contractions induced by histamine, acetylcholine and 5-hydroxytryptamine at concentrations that produced one-half maximal contractile response (ED50). Similarly S-Th combinations interacted in an additive manner to reverse histamine and acetylcholine contractions. In the case of both E-Th and S-Th combinations, the drugs were more effective in reducing the smooth muscle contractions when given during rather than prior to the response. It may be concluded that beta-sympathomimetics and methylxanthines when combined do not interact in a synergistic fashion to produce relaxation of contracted airway smooth muscle.

Acetylcholine↗

PubMed2002

Effects of transient muscle contractions and stretching on the tendon structures in vivo.

This study compared the effects of static stretching (ST) and repeated muscle contractions (CON) on the viscoelastic properties of tendon structures in vivo. Eight male subjects performed ST (passively flexed to 35 of dorsiflexion) for 5 min and 50 repetitions of isometric maximum voluntary contraction (MVC) for 3 s each with 3 s relaxation. Before and after each task, the elongation of the tendon and aponeurosis of the medial gastrocnemius muscle (MG) was directly measured by ultrasonography, while the subjects performed ramp isometric plantar flexion up to MVC, followed by a ramp relaxation. The relationship between the estimated muscle force (Fm) and tendon elongation (L) during the ascending phase was applied to a linear regression, the slope of which was defined as stiffness of the tendon structures. The percentage of the area within the Fm-L loop to the area beneath the curve during the ascending phase was calculated as an index representing hysteresis. The ST protocol significantly decreased the stiffness (-8%) and hysteresis (29%)., respectively. In contrast, the CON protocol significantly decreased the stiffness, but not the hysteresis. These results suggested that the stretching and repeated contractions would make the tendon structures more complaint, and further decreased the hysteresis of the tendon structures.

Adult↗

PubMed1986

Muscle-contraction headaches in multiple-pain patients: treatment under worsening baseline conditions.

A total of 55 muscle-contraction headache patients were divided into four groups which received frontalis EMG biofeedback, relaxation training, combined biofeedback-relaxation training, or no-treatment control. All patients were compensation patients undergoing assessment and brought to a high level of activity for the first time since going into chronicity. In all cases, onset or aggravation of the headaches coincided with the compensation-related injury. All treatment modalities led to significant but similar levels of improvement in headaches, while the control group worsened.

Adult↗

PubMed1989

[Heart insufficiency. Physiology and physiopathology of muscle contraction of the heart].

To understand physiopathology of contractibility in heart failure is needed the previous knowledge of normal muscle contractibility, calcium regulation, methods of assessment of isolated cardiac muscle and in situ heart contraction. Models of calcium movements during rest and contraction are presented and concepts of preload, afterload, Vmax and Po introduced. The importance of assessment of cardiac diastolic function is referred. Biochemical alterations in the failing myocardium are presented.

Calcium↗

PubMed1994

Adaptive cancellation of muscle contraction interference in vibroarthrographic signals.

Vibroarthrography (VAG) is an innovative, objective, non-invasive technique for obtaining diagnostic information concerning the articular cartilage of a joint. Knee VAG signals can be detected using a contact sensor over the skin surface of the knee joint during knee movement such as flexion and/or extension. These measured signals, however, contain significant interference caused by muscle contraction that is required for knee movement. Quality improvement of VAG signals is an important subject, and crucial in computer-aided diagnosis of cartilage pathology. While simple frequency domain high-pass (or band-pass) filtering could be used for minimizing muscle contraction interference (MCI), it could eliminate possible overlapping spectral components of the VAG signals. In this work, an adaptive MCI cancellation technique is presented as an alternative technique for filtering VAG signals. Methods of measuring the VAG and reference signals (MCI) are described, with details on MCI identification, characterization, and step size optimization for the adaptive filter. The performance of the method is evaluated by simulated signals as well as signals obtained from human subjects under isotonic contraction.

Adult↗

PubMed1999

[Probable involvement of the augmented agonist-induced Ca2+ sensitization of airway smooth muscle contraction in the pathogenesis of airway hyperresponsiveness].

Nonspecific airway hyperresponsiveness (AHR) is a common feature of allergic bronchial asthmatics, but the underlying mechanism (s) of AHR have yet to be elucidated. The importance of AHR in the pathogenesis of asthma has been suggested by its relevance to the severity of this disease. There is thus a need to understand the underlying mechanisms of AHR for the sake of asthma therapy. In the present minireview, we discussed the involvement of the augmented agonist-induced Ca2+ sensitization of airway smooth muscle contraction in the pathogenesis of AHR. Treatment with acetylcholine (ACh) of a beta-escin-permeabilized intrapulmonary bronchial smooth muscle of the rat induced a stronger contractile force even when the Ca2+ concentration was clamped at 1 microM. The ACh-induced Ca2+ sensitization of myofilaments was found to be significantly greater in antigen-induced airway hyperresponsive rats than in control rats. The ACh-induced Ca2+ sensitization was completely blocked by treatment with Clostridium botulinum C3 exoenzyme, an inactivator of the Rho family proteins. Moreover, the protein level of RhoA in the intrapulmonary bronchi was demonstrated to be significantly increased in the airway hyperresponsive rats. Thus, the increased airway smooth muscle contractility observed in asthmatics may be related to the augmented agonist-induced, Rho-mediated Ca2+ sensitization of myofilaments.

Acetylcholine↗

PubMed1998

Rho A regulates sustained smooth muscle contraction through cytoskeletal reorganization of HSP27.

The ras-related protein Rho p21 regulates various actin-dependent functions, including smooth muscle contraction. However, the precise mechanism of action of Rho p21 is still not clear. We report here that Rho A is a key regulator of agonist-induced contractile effects in rabbit colonic smooth muscle. Endothelin-1 and C2 ceramide were used. Both seem to activate phosphoinositide 3-kinase (PI 3-kinase) through G protein and pp60(src), respectively. Immunoprecipitation and immunoblotting revealed one form of 21-kDa Rho A that translocated from the cytosol to the membrane in response to stimulation by either endothelin (10(-7) M) or ceramide (10(-7) M) ( approximately 30% increase at 30 s that was sustained at 4 min). The translocation of Rho A to the membrane was confirmed by immunostaining. The translocation of Rho A was inhibited by Clostridium botulinum C3 exoenzyme, which ADP ribosylated Rho A, but was not inhibited by the pp60(src) inhibitor herbimycin A or by the protein kinase C (PKC) inhibitor calphostin C, suggesting that Rho A may be upstream of pp60(src) and PKC or may belong to a different pathway than these proteins. Both ceramide- and endothelin-induced PI 3-kinase activation was inhibited by C3 exoenzyme pretreatment. However, the C3 exoenzyme inhibited endothelin- but not ceramide-induced mitogen-activated protein kinase phosphorylation, indicating that Rho regulates ceramide- and endothelin-induced contraction through different pathways. Furthermore, the dominant negative form of Rho (N19Rho) inhibited the actin binding protein, 27-kDa heat shock protein (HSP27), reorganization in response to ceramide and endothelin observed under confocal microscopy.

ADP Ribose Transferases↗

PubMedDate not supplied

Direct action of 4-aminopyridine on the contractility of a fast-contracting muscle in the cat.

1. The effects of 4-aminopyridine on the contractility of the fast-contracting tibialis anterior and the slow-contracting soleus muscles of cats under chloralose anaesthesia have been studied. 2. 4-Aminopyridine, in doses of 0.5 mg/kg and above, produced a slowly developing increase in the twitch tension of directly stimulated chronically denervated and of indirectly stimulated innervated tibialis anterior muscles, but had little or no effect on twitches of soleus muscles. The effect of innervated tibialis anterior muscles was more pronounced than that on chronically denervated muscles, but it was nevertheless concluded that the whole effect on innervated muscles was the result of a direct action on the muscle fibres. The simultaneously occurring facilitatory action on neuromuscular transmission, which is manifested in the anti-curare action of 4-aminopyridine, had a faster time-course and occurred in both the tibialis anterior and the soleus muscles. 3. 4-Aminopyridine antagonized dantrolene sodium on on the tibialis anterior muscle but not on the soleus muscle. The antagonism could be described as physiological antagonism since it simply reflected the opposing actions on contractility of the two drugs. 4. 4-Aminopyridine was without effect on maximal tetanic tension of either the tibialis anterior or the soleus muscle. 5. It seems clear from the literature that a species difference exists with regard to the ability of 4-aminopyridine to increase muscle contractility. The results described in this paper show that muscle differences within the same species also exist.

4-Aminopyridine↗

PubMed2001

Muscle contraction and relaxation described by tactile stiffness.

We developed a tactile sensor system that measures the stiffness of objects (tactile stiffness) and used it to describe the time course of muscle contraction and relaxation. We examined fatigue resistance of the latissimus dorsi muscle (LDM), which is preconditioned for cardiomyoplasty. Time to peak, ripple of LDM, and time constant were calculated from the time course of LDM contraction and relaxation as described by tactile stiffness. We compared conditioned and unconditioned LDMs using these 3 parameters. The time course can be described by tactile stiffness. Tactile stiffness fell exponentially during LDM relaxation. In mean values, time to peak increased 230%, ripple decreased 20%, and time constants increased 424%. Significant differences were shown in 3 parameters between conditioned and unconditioned LDMs (p < 0.05). Our tactile sensor system can describe the time course of LDM contraction and relaxation. Examining the difference in time courses, we might detect the level of LDM preconditioning for cardiomyoplasty.

Animals↗

PubMed1990

Reflex responses of renal nerve activity during isometric muscle contraction in cats.

Renal sympathetic nerve activity (RSNA), arterial blood pressure (AP), and heart rate (HR) were measured during isometric muscle contraction of a hindlimb in chloralose-anesthetized cats. In 14 cats RSNA, AP, and HR increased during a 1-min contraction by 45%, 39 mmHg, and 11 beats/min, respectively; however, in three cats there was a brief initial decrease in RSNA followed by an increase. In 11 cats isometric contraction was maintained for 5 min by alternate stimulation of the L7 and S1 ventral roots. In the first 1 min of sustained contraction, there was a positive correlation (gamma = 0.58, P less than 0.005) between RSNA and tension development. Thereafter RSNA remained elevated despite a tension decrease, and there was no significant correlation between these changes. The RSNA response to contraction of both hindlimbs was greater than that to contraction of either hindlimb alone. Passive stretch of the hindlimb muscle significantly increased RSNA. Thus the initial increase in RSNA during sustained contraction is likely due to activation of muscle mechanoreceptors, whereas the later increase is probably caused by activation of the muscle metaboreceptors.

Animals↗

PubMed1997

Mechanisms by which insulin and muscle contraction stimulate glucose transport.

Insulin binding to its receptor activates a tyrosine kinase that initiates a cascade of signaling events, the initial step being the tyrosine phosphorylation of insulin receptor substrate 1 (IRS-1). Subsequent IRS-1 association and activation of phosphatidylinositiol 3-kinase (PI 3-kinase) is believed to be involved in the events leading to the translocation of glucose transporters (GLUT4) to the plasma membrane resulting in uptake of glucose into the cell. Muscle contractions increase insulin sensitivity, but also stimulate muscle glucose uptake independent of insulin. The contraction signaling pathway is distinct from the insulin pathway because the effect of insulin and contractions on glucose uptake are additive, and contractions do not increase insulin receptor kinase or PI 3-kinase activity. In contrast, studies indicating that contractions cause the translocation of GLUT4 and that both contractions and insulin-stimulated glucose transport can be blocked by calcium channel blockers suggest that the two pathways may converge. However, the possibility that two distinct GLUT4 pools may be targeted, one by insulin the other by contractions, indicates that additional research is needed to better define the mechanisms by which glucose transport is stimulated in muscle.

Animals↗

PubMed1952