Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Muscle Relaxation”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,099 records · Page 61Linked to original sources
PubMed1990

Striated scallop muscle relaxation: fast force transients produced by photolysis of Diazo-2.

Relaxation of the myosin regulated striated adductor muscles of Pecten maximus was initiated by the photolysis of the caged Ca2+ chelator, Diazo-2. The fibres relaxed to approximately 30% of the maximum tension with a mean half-time of 17.9 +/- 1.6 ms (n = 7, temp 12 degrees C), much faster than the rates observed in intact muscle at the same temperature. This indicates that in the intact adductor muscle the slower relaxation rate is determined by the speed of Ca2+ removal from the sarcoplasm. The faster rate of relaxation of scallop muscle in vitro, compared with frog skeletal muscle may reflect different mechanisms of regulation of the crossbridge cycle.

Animals↗
PubMed1990

[Potentiation of nondepolarizing muscle relaxants by nifedipine iv in inhalation anesthesia].

Calcium entry blockers are now widely used in the treatment of cardiovascular diseases. Nifedipine is established for the treatment of perioperative hypertension during anesthesia. Previous animal experiments have demonstrated that calcium entry blockers potentiate the neuromuscular response induced by nondepolarizing blocking drugs. Occasional observations in patients have led to the suggestion that this phenomenon may be of clinical significance. The interaction of nifedipine with nondepolarizing muscle relaxants in patients was assessed in a prospective clinical study. PATIENTS AND METHODS. Atracurium or vecuronium was administered for muscular relaxation in 44 patients anesthesized with isoflurane in nitrous oxide/oxygen. Monitoring included checks on noninvasive blood pressure, heart rate, pharyngeal temperature, tidal volume, end-tidal CO2 and neuromuscular transmission with a Datex ABM 100 Relaxograph ("train of four"). In the first study protocol atracurium was given to the patients after the intubation dose of 0.5 mg/kg in equal repetition doses of 0.2 mg/kg whenever T1 reached 25%. In 12 patients with the second repetition dose 1 mg nifedipine was injected i.v. The duration of neuromuscular depression with nifedipine until T1 reached 25% again was compared with the duration without nifedipine in the same patient. In the second protocol, constant neuromuscular blockade was accomplished in 11 patients by administration of atracurium or vecuronium at a constant perfusion rate at a level of 75% twitch depression. After 15 min of stable neuromuscular blockade 1 mg nifedipine was injected. In the third study protocol, 1 mg nifedipine i.v. was given at the end of anesthesia when the patients began to breathe spontaneously (T1 was at least 25%). RESULTS. In each patient there was a significant prolongation of neuromuscular blockade from 29 min +/- 6 min up to 40 min +/- 8 min when nifedipdine was given with the second repetition dose (P less than 0.001). During continuous relaxation with constant neuromuscular depression nifedipine increased the neuromuscular blockade from 75% up to 90% +/- 4% (P less than 0.05). In patients with spontaneous breathing and fading but still existing neuromuscular blockade nifedipine injection resulted in hypoventilation. The cardiovascular effects of 1 mg nifedipine, although significant, attained no clinically relevant values. CONCLUSIONS. Our results confirm previous assumptions of synergistic effects of neuromuscular blocking drugs and nifedipine in patients. This synergistic effect includes both duration and intensity of neuromuscular blockade. In the postoperative period patients may be endangered by nifedipine therapy if recovery from the neuromuscular depression is not complete.

Adult↗
PubMed1996

[Muscle relaxation with atracurium in myasthenia gravis].

This report concerns a narcosis in a 42-year-old female patient suffering from myasthenia gravis in a state of clinical remission after thymectomia. Six months after thymectomia relaxometric control (Datex AMG) was performed while the patient underwent major colorectal surgery. We found a persisting sensitivity to relaxants during isoflurane anaesthesia supplemented with fentanyl. During 270 minutes of anaesthesia we needed only 25 mg atracurium (0.4 mg/kg bodyweight) only 57% of a theoretical normal dose. This is the result of a continuing muscular weakness in asymptomatic patients suffering from clinically reliable myasthenia gravis. Therefore, a reduced demand for muscle relaxants can be expected in these patients.

Adult↗
PubMed1974

Tetanus: conservative management made easier by combination of muscle relaxants.

Conservative management of 11 consecutive cases of tetanus with diazepam in heavy doses and methocarbamol is described. All drugs were administered intravenously through a cut-down. Patients were nursed near the nurses' station for the first 3 to 5 days when fatal complications and very severe spasms are most likely to occur. There was minimal interference with the patients and a reasonable reduction in the duration of significant spasms, and complications were minimized. No neonates were included. Severity of tetanus cannot be determined only by consideration of onset of symptoms before admission. It is suggested that a combination of muscle relaxants without heavy sedation may produce an improvement in the results of conservative management of clinical tetanus.

Adolescent↗
PubMed2005

Arginase attenuates inhibitory nonadrenergic noncholinergic nerve-induced nitric oxide generation and airway smooth muscle relaxation.

BACKGROUND: Recent evidence suggests that endogenous arginase activity potentiates airway responsiveness to methacholine by attenuation of agonist-induced nitric oxide (NO) production, presumably by competition with epithelial constitutive NO synthase for the common substrate, L-arginine. Using guinea pig tracheal open-ring preparations, we now investigated the involvement of arginase in the modulation of neuronal nitric oxide synthase (nNOS)-mediated relaxation induced by inhibitory nonadrenergic noncholinergic (iNANC) nerve stimulation. METHODS: Electrical field stimulation (EFS; 150 mA, 4 ms, 4 s, 0.5 - 16 Hz)-induced relaxation was measured in tracheal preparations precontracted to 30% with histamine, in the presence of 1 microM atropine and 3 microM indomethacin. The contribution of NO to the EFS-induced relaxation was assessed by the nonselective NOS inhibitor L-NNA (0.1 mM), while the involvement of arginase activity in the regulation of EFS-induced NO production and relaxation was investigated by the effect of the specific arginase inhibitor nor-NOHA (10 microM). Furthermore, the role of substrate availability to nNOS in EFS-induced relaxation was measured in the presence of various concentrations of exogenous L-arginine. RESULTS: EFS induced a frequency-dependent relaxation, ranging from 6.6 +/- 0.8% at 0.5 Hz to 74.6 +/- 1.2% at 16 Hz, which was inhibited with the NOS inhibitor L-NNA by 78.0 +/- 10.5% at 0.5 Hz to 26.7 +/- 7.7% at 8 Hz (P < 0.01 all). In contrast, the arginase inhibitor nor-NOHA increased EFS-induced relaxation by 3.3 +/- 1.2-fold at 0.5 Hz to 1.2 +/- 0.1-fold at 4 Hz (P < 0.05 all), which was reversed by L-NNA to the level of control airways in the presence of L-NNA (P < 0.01 all). Similar to nor-NOHA, exogenous L-arginine increased EFS-induced airway relaxation (P < 0.05 all). CONCLUSION: The results indicate that endogenous arginase activity attenuates iNANC nerve-mediated airway relaxation by inhibition of NO generation, presumably by limiting L-arginine availability to nNOS.

Acetylcholine↗
PubMed1979

Studies on muscle relaxants during haemodialysis.

Signs of neuromuscular block were evident more than 20 hours after the administration of alcuronium to an anuric patient. Complete recovery occurred during haemodialysis. We therefore decided to study the dialysance of three radioactive non-depolarising relaxants during haemodialysis of four patients with chronic renal failure. Although dimethyl tubocurarine and alcuronium were equal as regards dialysance, the concentration of the former, in plasma, falls faster than does alcuronium. It is believed that a larger volume of distribution occurs with dimethyl tubocurarine. In spite of the fact that the dialysance of muscle relaxants is small, haemodialysis might lower the concentration of these substances in the plasma to a level below the critical point which produces paralysis.

Acute Kidney Injury↗
PubMed1997

Ectopic expression of phospholamban in fast-twitch skeletal muscle alters sarcoplasmic reticulum Ca2+ transport and muscle relaxation.

There are three isoforms of the sarcoplasmic reticulum Ca2+-ATPase; they are known as SERCA1, SERCA2, and SERCA3. Phospholamban is present in tissues that express the SERCA2 isoform and is an inhibitor of the affinity of SERCA2 for calcium. In vitro reconstitution and cell culture expression studies have shown that phospholamban can also regulate SERCA1, the fast-twitch skeletal muscle isoform. To determine whether regulation of SERCA1 by phospholamban can be of physiological relevance, we generated transgenic mice that ectopically express phospholamban in fast-twitch skeletal muscle, a tissue normally devoid of phospholamban. Ectopic expression of phospholamban was associated with a decrease in the affinity of SERCA1 for calcium. Assessment of isometric twitch contractions of intact fast-twitch skeletal muscles revealed depressed rates of relaxation in transgenic mice compared with wild-type cohorts. Furthermore, the prolongation of muscle relaxation appeared to correlate with the levels of phospholamban expressed in two transgenic mouse lines. These findings indicate that ectopic expression of phospholamban in fast-twitch skeletal muscle is associated with inhibition of SERCA1 activity and decreased relaxation rates of this muscle.

Adrenergic beta-Agonists↗
PubMed1979

Muscle relaxation in mechanically ventilated infants.

We evaluated the effect of muscle paralysis on gas exchange and incidence of pneumothorax in 35 severely ill infants on mechanical ventilation. Pancuronium (0.1 mg/kg) was given repeatedly until spontaneous respirations ceased in infants with inadequate gas exchange with FIO2 greater than 0.60, or peak inspiratory pressure greater than 30 cm H2O, or who were breathing out of phase with the respirator. Of 27 infants who had an alveolar-arterial oxygen gradient greater than 300 torr before paralysis, AaDO2 improved by greater than 100 torr within one hour of paralysis in only two infants; it worsened in two infants within the same period. By six hours postparalysis, 12 of 27 infants had improved, five of whom had had a worsening AaDO2 before administration of pancuronium. Changes in oxygenation were unrelated to changes in arterial carbon dioxide tension in most infants. Peak transpulmonary pressures after paralysis were lower than during spontaneous breathing, and may explain the low incidence of pneumothorax (3 of 35) during paralysis. Since those who improved could not be distinguished by birth weight, gestational age, or diagnosis, pancuronium might be worthy of trial in a mechanically ventilated infant with severe lung disease who is at risk for pneumothorax.

Carbon Dioxide↗
PubMed1996

Smooth muscle relaxing compounds from Dodonaea viscosa.

Bioassay-directed fractionation of the chloroform-methanol (1:1) extract of Dodonaea viscosa (L.) Jacq. (Sapindaceae) resulted in the isolation of four active spasmolytic principles: sakuranetin (1), 6-hydroxykaempferyl 3,7-dimethyl ether (2) hautrivaic acid (3), and ent-15, 16-epoxy-9 alpha H-labda-13(16)14-diene-3 beta, 8 alpha-diol (4). All the isolated compounds elicited a concentration-dependent inhibition of the spontaneous and electrically-induced contractions of guinea-pig ileum. Sakuranetin and the ent-labdane inhibited ileum contractions evoked by acetylcholine (Ach), histamine, and barium chloride. In addition, both substances were capable of relaxing contractions of rat uterus induced by Ca2+ in K(+)-depolarizing solution, displacing to the right the concentration-response curves to Ca2+. These results suggest that sakuranetin and ent-15,16-epoxy-9 alpha H-labda-13(16)14-diene-3 beta, 8 alpha-diol produce an interference with calcium metabolism in smooth muscle cells. The spasmolytic activity exhibited by the active principles from D. viscosa, provides the pharmacological basis for the traditional use of the plant as an antispasmodic agent.

Animals↗
PubMed1982

The effect of a benzodiazepine, flurazepam, on the response of in vitro skeletal muscle preparations to muscle relaxants: are purines or their receptors involved?

Changing trends in the use of anxiolytic agents and recent reassessment of their neuropharmacological activity has prompted this evaluation of the peripheral neuromuscular activity of the benzodiazepine, flurazepam. In previous reports we have documented peripheral neuromuscular activity of chlordiazepoxide and diazepam on the rat phrenic nerve diaphragm preparation. The water soluble benzodiazepine, flurazepam, has been studied on the rat phrenic nerve diaphragm and frog rectus abdominis in vitro. On the former preparation flurazepam enhanced and then blocked the response to indirect electrical stimulation (0.2 Hz) and readily blocked posttetanic potentiation and prevented the preparation from sustaining a tetanic contracture (30 Hz). On the later preparation, flurazepam blocked in a noncompetitive manner the response of the frog muscle to applied cholinergic agonists. Studies on the rat preparation with the neuromuscular blocking drug succinylcholine have shown an unexpected protection against blockade in preparations pretreated with low concentrations of flurazepam. This was not observed when flurazepam was given prior to d-tubocurarine. The application of adenosine to rat diaphragms during steady-state partial blockade caused by flurazepam or d-tubocurarine showed an inhibiting action of adenosine which was reversed by theophylline. Pretreatment of rat preparations with dipyridamole significantly enhanced the blocking action of standard concentrations of succinylcholine. These results, along with those in the literature, encourage a reassessment of the action of purines and benzodiazepines on skeletal muscle and encourage a consideration of a possible involvement of purinergic neuromodulation of transmission which is unmasked when the safety factor for transmission is altered by muscle relaxants. The possible clinical significance of protection against succinylcholine by benzodiazepines is noted.

Adenosine↗
PubMed1993

Comparative study of the rat uterine smooth muscle relaxant activity of three bisbenzyltetrahydroisoquinolines with tetrandrine.

The relaxant activity of three bisbenzyltetrahydroisoquinolines--obaberine, popisonine and lindoldhamine--was examined in rat isolated uterus and their inhibitory potencies were compared with that of tetrandrine. All alkaloids tested relaxed KCl-depolarized rat uterus and totally or partially inhibited oxytocin-induced rhythmic contractions. The degree of methylation of the free phenolic hydroxy groups and the loss of one diarylether bridge influence the potency of relaxant action of these alkaloids. Only alkaloids with absolute configuration 1R,1'S or 1R1'R acted intracellularly, promoting relaxation of contractile responses induced by oxytocin or vanadate in a Ca(2+)-free medium.

Alkaloids↗
PubMed1975

Effects of potassium chloride and smooth muscle relaxants on tension and cyclic nucleotide levels in rat myometrium.

Ten minutes after KCl-depolarization of rat myometrial strips, at which time the muscles were in a state of sustained contracture, tissue levels of adenosine 3',5'-cyclic monophosphate (cyclic AMP) were increased by approximately 40% over relaxed controls, and levels of guanosine 3',5'-cyclic monophosphate (cyclic GMP) were decreased by 40%. At this point both nitroglycerin (4 X 10(-4) M) and papaverine (2 X 10(-5) M) were capable of relaxing the depolarized muscles without significantly increasing cyclic AMP levels. Isoproterenol, in concentrations from 5 X 10(-9) M to 10(-6) M, relaxed the depolarized muscles and significantly increased tissue levels of cyclic AMP. However, the magnitudes of the cyclic AMP increases seen after the lower concentrations of isoproterenol were small relative to the increases observed during KCl-contracture alone. For example, the 40% elevation of cyclic AMP seen 10 min after KCl-depolarization did not cause the muscles to relax, whereas 5 X 10(-9) M isoproterenol caused relaxation with an increase in cyclic AMP levels of only 16% over depolarized controls. It was concluded that changes in total tissue levels of cyclic AMP were not responsible for the uterine relaxation caused by nitroglycerin, papaverine or isoproterenol in these experiments. Cyclic GMP levels in the depolarized muscles were not significantly changed by isoproterenol or papaverine but were increased approximately 80% by nitroglycerin. The above results are not consistent with the previously suggested roles for cyclic GMP and cyclic AMP as mediators of smooth muscle contraction and relaxation, respectively.

Animals↗