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PubMed2004

Sarcomeric determinants of striated muscle relaxation kinetics.

Ca2+ is the primary regulator of force generation by cross-bridges in striated muscle activation and relaxation. Relaxation is as necessary as contraction and, while the kinetics of Ca2+-induced force development have been investigated extensively, those of force relaxation have been both studied and understood less well. Knowledge of the molecular mechanisms underlying relaxation kinetics is of special importance for understanding diastolic function and dysfunction of the heart. A number of experimental models, from whole muscle organs and intact muscle fibres down to single myofibrils, have been used to explore the cascade of kinetic events leading to mechanical relaxation. By using isolated myofibrils and fast solution switching techniques we can distinguish the sarcomeric mechanisms of relaxation from those of myoplasmic Ca2+ removal. There is strong evidence that cross-bridge mechanics and kinetics are major determinants of the time course of striated muscle relaxation whilst thin filament inactivation kinetics and cooperative activation of thin filament by cycling, force-generating cross-bridges do not significantly limit the relaxation rate. Results in myofibrils can be explained well by a simple two-state model of the cross-bridge cycle in which the apparent rate of the force generating transition is modulated by fast, Ca2+-dependent equilibration between off- and on-states of actin. Inter-sarcomere dynamics during the final rapid phase of full force relaxation are responsible for deviations from this simple model.

Animals↗
PubMed1998

The actions of muscle relaxants at nicotinic acetylcholine receptor isoforms.

The pharmacological diversity of the different isoforms of the nicotinic acetylcholine receptor arises from the diversity of the subunits that assemble to form the native receptors. The aim of this study was to investigate the actions of the muscle relaxants d-tubocurarine, pancuronium and vecuronium on different isoforms of nicotinic acetylcholine receptors (mouse foetal muscle, mouse adult muscle and a rat neuronal), using the Xenopus oocyte expression system. Oocytes were injected with cRNAs for alpha, beta, gamma, delta subunits (the native foetal muscle subunit combination), or with cRNAs for alpha, beta, epsilon, delta subunits (the native adult muscle subunit combination), or with cRNAs for alpha4beta2 subunits (a putative native neuronal subunit combination). Acetylcholine had a similar potency at all three subunit combinations (EC50 11.6, 17.4 and 19.1 microM, respectively). At all three receptor types, d-tubocurarine and pancuronium blocked the responses elicited by acetylcholine in a reversible manner. Furthermore, the inhibition of the acetylcholine currents for the foetal and adult nicotinic acetylcholine receptor by pancuronium and d-tubocurarine was independent of the holding voltage over the range -100 to -40 mV. In oocytes expressing the foetal muscle nicotinic acetylcholine receptors the inhibition of the current in response to 100 microM acetylcholine by 10 nM d-tubocurarine was 29 +/- 5% (mean +/- S.E.M.; n = 7), and the inhibition by 10 nM pancuronium was 39 +/- 6% (mean +/- S.E.M.; n = 8; P > 0.05 vs. d-tubocurarine). However, in the adult form of the muscle nicotinic acetylcholine receptor, 10 nM d-tubocurarine and 10 nM pancuronium were both more effective at blocking the response to 100 microM acetylcholine compared to the foetal muscle nicotinic acetylcholine receptor, with values of 55 +/- 5% (P < 0.01; n = 12) and 60 +/- 4% (P < 0.001; n = 10), respectively. Thus the developmental switch from the gamma to the epsilon subunit alters the antagonism of the nicotinic acetylcholine receptor for both pancuronium and d-tubocurarine. Vecuronium was more potent than pancuronium. One nM vecuronium reduced the response to 100 microM acetylcholine by 71 +- 6% (n = 10) for foetal and 63 +/- 5% (n = 4) for adult nicotinic acetylcholine receptors. In the alpha4beta2 neuronal nicotinic acetylcholine receptor combination, 10 nM pancuronium was a more effective antagonist of the response to 100 microM acetylcholine (69 +/- 6%, n = 6) than 10 nM d-tubocurarine (30 +/- 5%; n = 6; P < 0.05 compared to pancuronium). This is in contrast to the adult muscle nicotinic acetylcholine receptor, where pancuronium and d-tubocurarine were equieffective. The expression of the beta2 subunit with muscle alpha, epsilon and delta subunits formed a functional receptor which was blocked by pancuronium and d-tubocurarine in a similar manner to the alphabeta1epsilondelta subunit consistent with the hypothesis that the beta subunit is not a major determinant in the action of this drug at the adult muscle nicotinic acetylcholine receptor.

Animals↗
PubMedDate not supplied

The effect of progressive muscle relaxation training on anxiety and quality of life after stoma surgery in colorectal cancer patients.

The aim of the study was to evaluate the effects of the use of progressive muscle relaxation training (PMRT) on anxiety and quality of life in colorectal cancer patients after stoma surgery. A randomised controlled trial was used with repeated measures assessment over 10 weeks post-stoma surgery. Fifty-nine patients participated in the study and were randomised to a control group receiving routine care (n=30) and an experimental group receiving routine care and PMRT through two teaching sessions and practice at home for the first 10 weeks. The State-Trait Anxiety Inventory and two Quality of Life Scales were used to collect the data of interest in three occasions, namely during hospitalisation, at week 5 and at week 10 post-surgery. The use of PMRT significantly decreased state anxiety and improved generic quality of life in the experimental group (P<0.05), especially in the domains of physical health, psychological health, social concerns and environment. Social relationships decreased in both groups. In relation to the disease-specific quality of life measure, differences were observed only in the 10-week assessment, with the experimental group reporting better quality of life at 10 weeks, but not over time as compared to the control group. The use of PMRT should be incorporated in the long-term care of colorectal cancer patients, as it can improve their psychological health and quality of life. This may be a cost-effective intervention that needs minimal training and could easily be offered to those patients that they would like to use it as part of the specialist care provided to stoma patients.

Analysis of Variance↗
PubMed1988

Anaphylaxis to muscle relaxants: cross-sensitivity studied by radioimmunoassays compared to intradermal tests in 34 cases.

Thirty-four patients (31 female and three male patients) with a previous anaphylactoid shock to muscle relaxants were investigated. The seric antimyorelaxant IgE was detected by radioimmunoassay (RIA), and the results were compared to intradermal test (IDR) reactions to dilutions of the commercial drugs. The RIA was carried out with a Sepharose-myorelaxant solid phase and anti-IgE 125I-labeled IgG. The results corresponded to the percentage of labeled anti-IgE bound on the solid phase. The RIA with Sepharose-alcuronium and Sepharose-choline was estimated positive from determination with normal sera (n = 12) when bound IgE was greater than 1.0% and 1.5%, respectively. The RIA and IDR were positive in 43.5% and 75%, respectively, of the cases, with a concordance of 66%. One test at least was positive in 79.4% of the cases. No correlation was found between IgE seric levels and the RIA nor between the cutaneous sensitivity and the RIA. Cross-reactivity with Sepharose-choline and Sepharose-alcuronium was observed in 50%, and it was demonstrated by IDR in only 34.2%. The RIA demonstrated the specificity of IgE to quaternary ammonium compounds as myorelaxant drugs. The positive IDR revealed the bridging of mast cell-bound specific IgE, depending on structural conditions, such as the flexibility of the molecules or the variable specificity of the antibodies, restricted to quaternary ammonium ions or enlarged to a broader part of the incriminated molecules.

Adolescent↗
PubMed1994

[The action of non-depolarizing muscle relaxants on nerve terminal of motor endplate--relationship between run-down of endplate potentials and fading tension response].

The classical view of the neuromuscular transmission is that non-depolarizing muscle relaxants (MRs) enhance run-down of the endplate potentials (epps) by blocking pre-junctional nicotinic acetylcholine (ACh) receptors. Several recent investigations, when extended to pharmacology, have provided evidence to suggest the existence of other types of enhancement of run-down of epps by MRs; the enhancement of epps occurs without reduction of ACh release in the presence of MRs. It has been generally accepted that the enhancement of run-down of epps causes the tetanic fade of tension response. However, recent evidence indicates that run-down of epps does not always cause this wane in tension. The electrophysiological mechanism of run-down of epps at the neuromuscular junction and the relationship between that phenomenon and the extent of reduction of tension response are described based on a review of literature and our current investigations.

Acetylcholine↗
PubMed2004

Metoclopramide causes airway smooth muscle relaxation through inhibition of muscarinic M3 receptor in the rat trachea.

UNLABELLED: Although metoclopramide, often used as an antiemetic, is reported to have an anticholinesterase action, the effect on airway smooth muscle remains unclear. We investigated the effect of metoclopramide on the contraction, phosphatidylinositol response, and binding affinity of muscarinic M(3) receptors in rat trachea preparations. Male Wistar rats were anesthetized and their tracheas excised and chopped into 3-mm-wide rings, 1-mm-wide slices, or frozen 10- microm-thick sections. Contraction was induced with 0.55 microM carbachol (CCh) and, 30 min later, metoclopramide (10 microM to 1 mM) was added. The slices were incubated with (3)[H]myo-inositol, 0.55 microM CCh, and metoclopramide, and the formation of (3)[H] inositol monophosphate was measured. A radioligand binding study was conducted to examine the effects of metoclopramide using [(3)H] 4-diphenylacetoxy-N-methyl-piperidine methobromide (4-DAMP), a muscarinic M(3) receptor antagonist, in sections of the trachea. Metoclopramide concentration dependently attenuated CCh-induced contraction and inositol monophosphate accumulation, and also attenuated the binding affinity of 4-DAMP to muscarinic M(3) receptors. The 50% inhibitory concentration of metoclopramide against the binding affinity of 4-DAMP to muscarinic M(3) receptors of rat trachea was 24 micro M. These findings suggest that the attenuation by metoclopramide of CCh-induced contraction and phosphatidylinositol response may be mediated through the muscarinic M(3) receptors. IMPLICATIONS: We investigated the effect of metoclopramide on the contraction, phosphatidylinositol response, and binding affinity of muscarinic M(3) receptors in rat trachea preparations. Our findings suggest that the attenuation by metoclopramide of carbachol-induced contraction and phosphatidylinositol response may be mediated through the muscarinic M(3) receptors.

Animals↗
PubMedDate not supplied

Pelvic muscle relaxation. Assessment and management.

Strong pelvic musculature is important to the health of women because of the role it plays in maintaining urinary continence and in providing support to the pelvic organs. Therefore, assessment for pelvic muscle relaxation and strategies for preventive and therapeutic management are necessary elements of care. This paper discusses several assessment techniques that were tested in research settings but that are readily transferable to clinical care. Research-based recommendations for nurse-midwifery management, with emphasis on effective teaching of pelvic muscle exercise, are made. Pelvic muscle exercise is a noninvasive technique that should be used as the initial treatment of urinary incontinence, before a surgical alternative is tried. Moreover, women with weaker pelvic musculature, who are identified early, can begin a program of preventive exercise that may help to avoid incontinence in later life.

Exercise↗
PubMed1985

[Change in skin reactivity in anaphylaxis to muscle relaxants and hypnotics after administration of anti H1, anti H2 and tritoqualine].

Inhibition of allergic skin reactivity was studied by the technique of thresholds in 35 patients presenting with an anaphylaxis to muscle relaxants. This method was useful to determine the anti-histamine or anti-anaphylactic effects of different substances. The best results were obtained with hydroxyzine. Associating it with an anti H2 drug (cimetidine or ranitidine) did not improve these results. Skin reactivity was never entirely abolished. This confirmed that no premedication could avoid the occurrence of an anaphylactic shock, or even reduce its magnitude. However, premedicating before general anaesthesia with anti H1 and anxiolytic drugs must be continued for all high risk patients: the prevention of non-specific histamine release appeared to be much more efficient than that of anaphylaxis.

Anaphylaxis↗
PubMed2002

Opposite actions of caffeine and creatine on muscle relaxation time in humans.

The effect of creatine and caffeine supplementation on muscle torque generation and relaxation was investigated in healthy male volunteers. Maximal torque (T(max)), contraction time (CT) from 0.25 to 0.75 of T(max), and relaxation time (RT) from 0.75 to 0.25 of T(max) were measured during an exercise test consisting of 30 intermittent contractions of musculus quadriceps (2 s stimulation, 2 s rest) that were induced by electrical stimulation. According to a double-blind randomized crossover design, subjects (n = 10) performed the exercise test before (pretest) and after (posttest) creatine supplementation (Cr, 4 x 5 g/day, 4 days), short-term caffeine intake (Caf, 5 mg x kg(-1) x day(-1), 3 days), creatine supplementation + short-term caffeine intake (Cr+Caf), acute caffeine intake (ACaf, 5 mg/kg) or placebo. Compared with placebo, Cr shortened RT by approximately 5% (P < 0.05). Conversely, Caf increased RT (+ approximately 10%, P < 0.05), in particular as RT increased because of fatigue. RT was not significantly changed by either Cr+Caf or ACaf. T(max) and CT were similar during all experimental conditions. Initial T(max) was approximately 20% of voluntary maximal isometric contraction force, which was not different between treatments. It is concluded that Caf intake (3 days) prolongs muscle RT and by this action overrides the shortening of RT due to creatine supplementation.

Adult↗
PubMed1998

Evidence that different mechanisms underlie smooth muscle relaxation to nitric oxide and nitric oxide donors in the rabbit isolated carotid artery.

1. The endothelium-dependent relaxants acetylcholine (ACh; 0.03-10 microM) and A23187 (0.03-10 microM), and nitric oxide (NO), applied either as authentic NO (0.01-10 microM) or as the NO donors 3-morpholino-sydnonimine (SIN-1; 0.1-10 microM) and S-nitroso-N-acetylpenicillamine (SNAP; 0.1-10 microM), each evoked concentration-dependent relaxation in phenylephrine stimulated (1-3 microM; mean contraction and depolarization, 45.8+/-5.3 mV and 31.5+/-3.3 mN; n=10) segments of rabbit isolated carotid artery. In each case, relaxation closely correlated with repolarization of the smooth muscle membrane potential and stimulated a maximal reversal of around 95% and 98% of the phenylephrine-induced depolarization and contraction, respectively. 2. In tissues stimulated with 30 mM KCl rather than phenylephrine, smooth muscle hyperpolarization and relaxation to ACh, A23187, authentic NO and the NO donors were dissociated. Whereas the hyperpolarization was reduced by 75-80% to around a total of 10 mV, relaxation was only inhibited by 35% (n=4-7 in each case; P<0.01). The responses which persisted to ACh and A23187 in the presence of 30 mM KCl were abolished by either the NO synthase inhibitor L-NG-nitroarginine methyl ester (L-NAME; 100 microM) or the inhibitor of soluble guanylyl cyclase 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 10 microM; 10 min; n=4 in each case; P<0.01). 3. Exposure to ODQ significantly attenuated both repolarization and relaxation to ACh, A23187 and authentic NO, reducing the maximum changes in both membrane potential and tension to each relaxant to around 60% of control values (n=4 in each case; P<0.01). In contrast, ODQ almost completely inhibited repolarization and relaxation to SIN-1 and SNAP, reducing the maximum responses to around 8% in each case (n=3-5; P<0.01). 4. The potassium channel blockers glibenclamide (10 microM), iberiotoxin (100 nM) and apamin (50 nM), alone or in combination, had no significant effect on relaxation to ACh, A23187, authentic NO, or the NO donors SIN-1 and SNAP (n=4 in each case; P>0.05). Charybdotoxin (ChTX; 50 nM) almost abolished repolarization to ACh (n=4; P<0.01) and inhibited the maximum relaxation to ACh, A23187 and authentic NO each by 30% (n=4-8; P<0.01). Application of ODQ (10 microM; 10 min) abolished the ChTX-insensitive responses to ACh, A23187 and authentic NO (n=4 in each case; P<0.01 5. When the concentration of phenylephrine was reduced (to 0.3-0.5 microM) to ensure the level of smooth muscle contraction was the same as in the absence of potassium channel blocker, ChTX had no effect on the subsequent relaxation to SIN-1 (n=4; P>0.05). However, in the presence of tone induced by 1-3 microM phenylephrine (51.2+/-3.3 mN; n=4), ChTX significantly reduced relaxation to SIN-1 by nearly 50% (maximum relaxation 53.2+/-6.3%, n=4; P<0.01). 6. These data indicate that NO-evoked relaxation of the rabbit isolated carotid artery can be mediated by three distinct mechanisms: (a) a cyclic GMP-dependent, voltage-independent pathway, (b) cyclic GMP-mediated smooth muscle repolarization and (c) cyclic GMP-independent, ChTX-sensitive smooth muscle repolarization. Relaxation and repolarization to both authentic and endothelium-derived NO in this large conduit artery appear to be mediated by parallel cyclic GMP-dependent and -independent pathways. In contrast, relaxation to the NO-donors SIN-1 and SNAP appears to be mediated entirely via cyclic GMP-dependent mechanisms.

Acetylcholine↗