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At least 847 records · Page 47Linked to original sources
PubMed1963

The nature of the muscle-relaxing factor. I. An improved assay system.

Analysis of the effects of deoxycholate and benzalkonium chloride on granule relaxing activity, myofibril and glycerinated fiber responses to ATP, and the sensitivity of these actomyosin-containing systems to relaxing factors have established that it is possible to differentially inactivate intrinsic granule relaxing factor. It is therefore possible to use these agents to treat myofibrils and glycerinated muscle fibers so that they may be used for the assay of muscle-relaxing factor preparations. The destruction of intrinsic relaxing factor can be produced by treating actomyosin with 1 mM deoxycholate or 0.005 per cent benzalkonium chloride for 5 minutes at room temperature.

Actomyosin↗
PubMed1998

cGMP mediates corpus cavernosum smooth muscle relaxation with altered cross-bridge function.

We tested the prevailing paradigm that relaxation of corpus cavernosum smooth muscle (CCSM) and penile erection depends upon nitric oxide-induced elevation of myoplasmic cGMP and reduced Ca2+-dependent myosin regulatory light chain phosphorylation levels. This hypothesis invokes a reversal of normal activation pathways. Upon stimulation with 250 microM phenylephrine, phosphorylation of the 20 kD myosin regulatory light chains of rabbit or human CCSM increased approximately 4-fold coincident with contraction. Removal of the agonist was followed by a slow reduction in cross-bridge phosphorylation and force to basal levels. The NO donor, sodium nitroprusside elicited a dose-dependent increase in tissue [cGMP] associated with a rapid relaxation in the continued presence of phenylephrine, although cross-bridge phosphorylation remained significantly elevated. Thus the NO-cGMP inhibitory pathway in CCSM is not simply a reversal of excitatory signal transduction mechanisms. An unidentified mechanism contributes to relaxation by decreasing the rate of cross-bridge recruitment through phosphorylation.

Animals↗
PubMed1981

Mechanisms underlying the prolonged duration of action of muscle relaxants caused by extrahepatic cholestasis.

The neuromuscular blocking effects of Org 6368 and Org NC 45 were studied in rats with experimental cholestasis and in controls. The effect of Org NC 45 during infusion of taurocholate was investigated. In cholestatic rats we observed a three-fold increase of the duration of action of Org 6368 and Org NC 45. The same was observed for Org NC 45 with taurocholate. In the rat phrenic nerve-hemidiaphragm preparation taurocholate potentiated the neuromuscular blockade of Org 6368, pancuronium and gallamine, but not Org NC 45. Increased bile salt concentrations caused strong inhibition of hepatic uptake and biliary excretion of Org 6368 and tubocurarine in isolated perfused livers. Taurocholate and glycocholate were more potent than cholate and chenodeoxycholate. Cholestatic livers exhibited a clearance of Org 6368 which was 50% of control. We conclude that the prolonged duration of action of certain muscle relaxants because of cholestasis results from both inhibition of hepatic uptake by the accumulated bile salts and a general deterioration of liver transport function.

Animals↗
PubMed2005

Short use of muscle relaxants following single stage laryngotracheoplasty in children.

OBJECTIVE: The postoperative management of children undergoing single stage laryngotracheoplasty (SSLTP) includes intubation and muscle paralysis to secure the airway and protect the wound. We reduced the period of postoperative muscle paralysis in an attempt to decrease the incidence of pulmonary complications. The objective of this study was to evaluate the influence of the duration of muscle paralysis on pulmonary complications and outcome. METHODS: Medical records of all children admitted, between 1994 and 2002, to the pediatric intensive care unit following SSLTP were analysed. Children were grouped according to the number of days muscle paralysis was used. RESULTS: Thirty-six children (15 male, 21 female, mean age 32 months (9-162 months)) underwent SSLTP for laryngeal stenosis. Prior to surgery 29 needed a tracheotomy (mean duration 11.1 months). Shorter muscle paralysis leads to shorter intubation and mechanical ventilation and therefore PICU and hospital length of stay were 12.4 and 9.9days shorter in the group with short use of muscle paralysis (p<0.001 and p=0.002, respectively). There was no significant difference in postoperative complications, but a trend towards fewer atelectases in children with short muscle paralysis could be recognised. Postoperatively we observed no auto-extubations in either group and success rate of SSLTP was comparable in both groups (94 and 95%). CONCLUSION: Children undergoing SSLTP can safely benefit from a postoperative strategy using a short duration of muscle relaxants. They have fewer days on mechanical ventilation with a concomitant decrease in duration of hospital stay.

Adolescent↗
PubMed1991

[Muscle relaxation using atracurium in porphyria variegata--case notes].

A case is presented involving the use of atracurium (120 mg) as a muscle relaxant in a patient with known variegate porphyria. The concentrations of urinary porphyrins and porphyrin precursors did not increase after this anaesthetic, and no exacerbation of the disease was noted. This single case suggests that atracurium can be used safely in patients with porphyria.

Atracurium↗
PubMed1991

Anaphylaxis to muscle-relaxant drugs: study of cross-reactivity by skin tests.

Intradermal skin tests (two dilutions) carried out systematically with 5 muscle-relaxant drugs were used to study the cross-reactivity between these drugs in 131 patients who had suffered from anaphylaxis. The skin tests were positive for at least 2 drugs in 65.6% of the cases. We observed a significant concordance (positive-positive or negative-negative skin tests) between pancuronium and vecuronium (p less than 0.01) and a significant correlation between the skin test diameters obtained with these 2 drugs (p less than 0.02 for wheals and p less than 0.01 for flares). Conversely, the lack of concordance between pancuronium and suxamethonium was significant (p less than 0.05). When comparing all the concordances obtained with each pair of drugs, it appeared that the concordance between pancuronium and vecuronium was significantly higher than all others. For other concordances, 2 main factors seemed to play a role: the N+ of the ammonium ions included in a ring as in pancuronium and the presence of a 'choline-like' side chain as in suxamethonium. But there was no significant correlation between skin test diameters. Altogether, these results suggest that in vivo there is no 'true' cross-reactivity between the drugs except frequently between pancuronium and vecuronium. In all other cases, the patients have probably specific IgE antibodies for each drug, all these antibodies being able to recognize the ammonium determinant; this common property may be insufficient to induce a clinical allergy.

Adolescent↗
PubMed1998

Airway hyperresponsiveness in asthma. Not just a problem of smooth muscle relaxation with inspiration.

Airway hyperresponsiveness in asthma has been attributed to impaired ability of deep inspiration (DI) to stretch airway smooth muscle. We have retested this hypothesis by comparing the responses to methacholine of 10 asthmatic and 10 control subjects. After each dose subjects breathed tidally without deep inspiration for 4 min, followed by a forced partial expiration from which flow was measured at a constant volume, 35% baseline VC (Vp 35). This index is independent of both DI and increases in end-inspiratory lung volume (EILV). EILV increased significantly more in the asthmatic group than in the control group (15.0 versus 2.5% of baseline VC, p = 0. 019), a factor that if not taken into account would tend to mask the difference in the two responses. Comparisons were made after a cumulative dose of 50 microg methacholine, which was the highest dose common to all subjects. The asthmatic response was significantly greater than that seen in the control group, with reductions to 25.9 and 72.1% of baseline Vp 35, respectively (p = 0. 0007). We conclude that the sensitivity of asthmatic airways to methacholine is greater than that of normal airways even when DI is prohibited. Therefore, the hyperresponsiveness of asthmatic airways is not attributable simply to an inability of DI to stretch airway smooth muscle.

Adult↗
PubMed1987

The effect of oral zindotrine (MDL-257), a bronchial smooth muscle relaxant, on histamine airways responsiveness in asymptomatic asthmatics.

We evaluated the efficacy of an oral dosage form of the investigational smooth muscle relaxant, zindotrine, a novel pyridazine derivative, in counteracting histamine-induced bronchospasm in a group of 12 non-medicated asymptomatic asthmatics. Histamine inhalation challenges were performed before (control) and 45, 150, and 300 minutes after zindotrine (200 and 300 mg), or the corresponding dose of placebo was administered orally in a randomized, double-blind crossover fashion. When compared to the control state, the 300-mg zindotrine dose markedly lowered histamine airway responsiveness as indicated by a significant (P less than .01) increase in the inhaled histamine dose necessary to provoke a 20% decrease in the forced expired volume in one second (PD20FEV1) 45 minutes after drug administration. The PD20FEV1 then decreased linearly over time but remained higher than the control PD20FEV1 value (P less than .05) during the entire observation period. The 200-mg zindotrine dose failed to affect the PD20FEV1. Our data indicate that orally administered zindotrine lowers airways responsiveness to inhaled histamine in asymptomatic asthmatics in a dose-dependent and time-dependent fashion.

Administration, Oral↗
PubMed1993

Role of Na(+)-K(+)-ATPase in airway smooth muscle relaxation by vasoactive intestinal peptide and pituitary adenylate cyclase activating peptide.

To elucidate the effects of vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase activating peptide (PACAP) on airway smooth muscle function, we studied rabbit isolated tracheal segments under isometric conditions in vitro. Addition of VIP and PACAP dose-dependently relaxed tracheal smooth muscle precontracted with acetylcholine, with the order potency being PACAP (1) > or = VIP (0.78), accompanied by the corresponding increase in intracellular cyclic AMP levels. The VIP- and PACAP-induced muscle relaxations were significantly inhibited by ouabain and K(+)-free medium. Incubation of tissues with VIP reduced the contractile responses to electrical field stimulation, whereas PACAP had no effect. These results suggest that VIP and PACAP may cause bronchodilation through activation of Na(+)-K(+)-ATPase and that VIP but not PACAP inhibits the release of acetylcholine from the cholinergic nerve terminals.

Acetylcholine↗