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At least 19 recordsLinked to original sources
PubMed1994

Protection by alcuronium of muscarinic receptors against chemical inactivation and location of the allosteric binding site for alcuronium.

We have found earlier that the neuromuscular blocker alcuronium binds to cardiac muscarinic receptors simultaneously with their specific antagonist [3H]methyl-N-scopolamine ([3H]NMS) and allosterically increases their affinity to this ligand. Nothing is known about the allosteric site with which alcuronium interacts. To gain an insight, we have now investigated how the binding of [3H]NMS is affected by agents known to modify specific residues in proteins and how their effects are altered by alcuronium. Reagents that covalently modify the tyrosyl residues (p-nitrobenzenesulfonyl fluoride and 4-chloro-7-nitrobenzofurazan) and the carboxyl groups of aspartate and glutamate [1-ethyl-3-(3-dimethylaminopropyl)carbodiimide, N,N'-dicyclohexylcarbodiimide, and N-ethyl-5-phenylisoxazolium-3'-sulfonate] blocked the binding of [3H]NMS to receptors in rat heart atria. Their action was probably due to the modification of tyrosyl and aspartyl residues directly in the muscarinic binding sites because it was antagonized by atropine and carbamoylcholine. Alcuronium and gallamine, another allosteric ligand, also protected the [3H]NMS binding sites against the inactivation by tyrosine- and carboxyl-directed chemical modifiers just as well as by benzilylcholine mustard, known to attach covalently to the muscarinic binding sites. Protection by alcuronium has also been observed on cerebrocortical muscarinic receptors. The effect of alcuronium indicates that the drug interferes with the access of chemical modifiers to the muscarinic sites. In view of the unspecific nature of most of the modifiers used (with regard to muscarinic mechanisms), the protection by alcuronium appears to be best explained on the assumption that the drug binds in close vicinity of the "classical" muscarinic site and sterically blocks the access to this site.

Acetylcholine↗
PubMed1994

Mechanisms of steric and cooperative actions of alcuronium on cardiac muscarinic acetylcholine receptors.

Kinetics of the interactions between the neuromuscular blocker alcuronium, the specific muscarinic antagonist N-[methyl-3H] methyl scopolamine ([3H]NMS), and muscarinic receptors were investigated in homogenates of rat heart atria. Two effects of alcuronium on the binding of [3H]NMS could be distinguished. (a) Alcuronium concentration-dependently slowed the association of [3H]NMS with receptors and the dissociation of [3H]NMS from receptors so that, at high alcuronium concentrations, equilibrium binding could not be reached, even after 20 hr, without special precautions. (b) Alcuronium increased the affinity of receptors for [3H]NMS, which was manifested by a decrease of the apparent Kd (> 3-fold) with no change in the Bmax for [3H]NMS binding. The effects of alcuronium on the rates of [3H]NMS association and dissociation can be explained only by a reaction mechanism in which [3H]NMS binds only to free receptors (not occupied by alcuronium), whereas alcuronium binds both to free receptors and to receptors occupied by [3H]NMS. Similarly, [3H]NMS cannot dissociate from receptors as long as alcuronium is attached to them. Experimental data agree with corresponding mathematical models. It is proposed that alcuronium blocks entry to the pocket containing the [3H]NMS binding site. In addition to this blocking effect, alcuronium has a positive allosteric effect on [3H]NMS binding, presumably by inducing a conformational change of the orthosteric muscarinic binding site. Earlier observations suggesting that, at high concentrations, alcuronium also competes for [3H]NMS binding sites can be explained by insufficient equilibration of the system.

Alcuronium↗
PubMed1990

[The dose-response relationship and time course of the neuromuscular blockade by alcuronium].

Although alcuronium has been in clinical use for almost 40 years, there is still considerable controversy in the literature regarding its neuromuscular blocking potency, the time course of the drug action and the side effects. The aim of this study was to investigate the dose-response relationship of alcuronium and to compare the time course of its neuromuscular effects with vecuronium following intubation doses of both compounds. METHODS. The study was carried out in two parts. In the first part 60 patients and in the second part 30 consenting ASA class I or II patients 20-60 years of age were included. The patients were undergoing elective gynecological or intra-abdominal operations. In the first part the patients received six different doses of alcuronium (60, 90, 120, 150, 180 or 210 micrograms/kg) in order to establish its dose-response relationship. Each dose was administered to ten patients. In the second part patients received either 300 micrograms/kg alcuronium (n = 15) or 100 micrograms/kg vecuronium (n = 15), and the time course of these two compounds (onset time, duration 25%, duration 75% and the recovery index) were compared. To test the reversibility, ten patients in each group received 30 micrograms/kg neostigmine at 25% recovery of T1. The neuromuscular effects of alcuronium and vecuronium were quantitated by EMG using the DATEX relaxograph. RESULTS. The log-logit analysis of the dose response data revealed an ED50 of 111 micrograms/kg and an ED95 of 250 micrograms/kg, which is in reasonable agreement with the measured effects following 120 micrograms/kg and 210 micrograms/kg alcuronium, resulting in 52 +/- 21% and 96 +/- 4% T1 depression, respectively. The onset time, duration 25%, duration 75% and spontaneous recovery index following 300 micrograms/kg alcuronium (5.0 +/- 3.4 min, 62 +/- 25 min, 119 +/- 38 min and 58 +/- 34 min) appeared to be significantly longer (P less than 0.05) than those observed after 100 micrograms/kg vecuronium (3.2 +/- 1.2 min, 33 +/- 7 min, 49 +/- 9 min and 18 +/- 7 min), respectively. The most striking finding of this study is the enormous individual variations observed in both neuromuscular potency and the time course of action of alcuronium. Following 150 micrograms/kg (routinely employed in daily clinical practice), the magnitude of T1 depression ranged between 19% and 100%. The same vast individual variations were observed in the time course of action following 300 micrograms/kg of alcuronium. The onset time, duration 25%, duration 75% and spontaneous recovery index ranged between 1.3 and 14 min, 22 and 110 min, 93 and 186 min and 32 and 116 min, respectively. CONCLUSIONS. The ED50 and ED95 values for alcuronium found in this study are in the same order of magnitude as 106.8 micrograms/kg and 135 micrograms/kg for ED50 and with 280 micrograms/kg for ED95, respectively, as reported by others. The long duration with slow recovery and the wide individual variation in the neuromuscular effects observed in our study have been reported earlier. Based on the above observations and because of the availability of better alternatives with fewer side effects, we conclude that alcuronium should be added to the list of obsolete neuromuscular blocking agents, together with gallamine and d-tubocurarine.

Adult↗
PubMed1990

Positive cooperativity in the binding of alcuronium and N-methylscopolamine to muscarinic acetylcholine receptors.

The effect of the neuromuscular blocker alcuronium on the binding of N-[3H]-methylscopolamine [( 3H]NMS) and l-[3H]quinuclidinylbenzilate ([3H]QNB) to muscarinic binding sites in rat heart atria, longitudinal smooth muscle of the ileum, cerebral cortex, cerebellum, and submaxillary glands was measured using filtration techniques. In the presence of 10(-5) M alcuronium, the binding of [3H]NMS (which was present at a subsaturating concentration of 2 x 10(-10) M) was increased 5.3-fold in the atria and smooth muscle and 3-fold in the cerebellum; no increase was observed in the brain cortex and salivary glands. The binding of [3H]NMS was inhibited at 10(-3) M and higher concentrations of alcuronium. The rates of [3H]NMS association to and dissociation from muscarinic binding sites in the atria were diminished by 10(-5) M alcuronium. Scatchard plots of [3H]NMS binding data obtained with and without 10(-5) M alcuronium indicated that the maximum number of binding sites was not altered by the drug, whereas the apparent Kd for [3H]NMS was diminished. In contrast to [3H] NMS, the effects of alcuronium on the binding of [3H]QNB were only inhibitory. The concentration of alcuronium required to diminish the binding of [3H]QNB by 50% (IC50) was 4-7 microM in the atria, ileal smooth muscle, and the cerebellum, 140 microM in the brain cortex, and 1200 microM in the parotid gland. The results suggest that the binding of low concentrations of alcuronium to muscarinic receptors in the heart, ileal smooth muscle, and cerebellum allosterically increases the affinity of muscarinic receptors towards [3H]NMS, although not [3H]QNB. At high concentrations, alcuronium inhibits the binding of muscarinic ligands, presumably by competition for the classical muscarinic binding site. Positive cooperativity induced by alcuronium appears to be specific for the m2 (cardiac) subtype of muscarinic receptors.

Alcuronium↗
PubMed1995

Subtype selectivity of the positive allosteric action of alcuronium at cloned M1-M5 muscarinic acetylcholine receptors.

The neuromuscular blocking drug alcuronium was found earlier to increase the affinity of muscarinic receptors for methyl-N-scopolamine (NMS). This effect could be observed in some but not in other tissues. Subtype selectivity of the positive allosteric action of alcuronium was now investigated in radioligand binding experiments in Chinese hamster ovary (CHO) cells stably transfected with the genes encoding the M1-M5 subtypes of muscarinic receptors. Alcuronium had a particularly high affinity for the M2 receptor subtype (Kd = 0.6 microM) and its affinity for muscarinic receptor subtypes diminished in the order M2 > M4 = M3 > M1 > M5. Alcuronium allosterically increased the binding of (3H)NMS to membranes containing receptors of the M2 (cooperativity factor alpha = 0.38) and M4 subtypes (alpha = 0.72) and inhibited the binding of (3H)NMS to membranes containing receptors of the M1, M3 and M5 subtypes (alpha = 3.35-4.35). The positive effects of alcuronium could also be observed in experiments with (3H)NMS binding to intact whole cells, indicating that the positive allosteric action of alcuronium occurs by alcuronium binding to receptor domains that are accessible from the extracellular space. Alcuronium diminished the affinity for (3H)quinuclidinyl benzilate [(3H)QNB] at all five subtypes of muscarinic receptors and slowed down the dissociation of both (3H)NMS and (3H)QNB; its decelerating effect on radioligand dissociation was most pronounced at the M2 receptor subtype. Differences between the effects of alcuronium on individual muscarinic receptor subtypes are apparently responsible for differences between the allosteric effects of alcuronium on muscarinic receptors in various tissues that had been described previously.

Alcuronium↗
PubMed2002

Allosteric modulation of muscarinic receptor signaling: alcuronium-induced conversion of pilocarpine from an agonist into an antagonist.

Previous studies on allosteric interactions at muscarinic receptors have often focused on ligand-receptor binding interactions, because ligand binding seemed to reflect functional consequences. The prototypal allosteric agent alcuronium is known to bind with similar affinity to the M(2) subtype of muscarinic acetylcholine receptors whether or not the receptors are occupied by the agonist pilocarpine. To determine allosteric modulation of receptor signaling by alcuronium, the effects of pilocarpine were measured in contracting guinea pig left atria and on G-protein coupling in M(2)-transfected Chinese hamster ovary (CHO) cell membranes. Alcuronium dose-dependently suppressed pilocarpine-induced reduction of isometric contraction force in atria (pIC(50, Alc) = 5.63) without any effect on the EC(50) of pilocarpine, consistent with an allosteric mechanism. In contrast, alcuronium shifted the concentration-effect curve of the agonist oxotremorine M to the right without affecting the maximal effect, in a formally competitive manner (pK(A, Alc) = 5.54). If pilocarpine remained receptor bound in the presence of alcuronium, this indicates that pilocarpine can no longer act as an agonist. In support of this hypothesis, pilocarpine acted as a competitive antagonist against oxotremorine M in the presence of 10 microM alcuronium. Measuring guanosine 5'-O-(3-[(35)S]thio)triphosphate ([(35)S]GTPgammaS) binding in CHO-M(2) membranes yielded similar results. Alcuronium suppressed pilocarpine-induced stimulation of [(35)S]GTPgammaS binding (pIC(50, Alc) = 5.47) without shift in EC(50), whereas it competitively shifted the response to oxotremorine M (pK(A, Alc) = 5.97). [(3)H]Oxotremorine M binding data corresponded with the functional findings. In conclusion, alcuronium converted the agonist pilocarpine into an antagonist-a novel type of functional allosteric interaction.

Alcuronium↗
PubMed1996

[Neuromuscular blockade after atracurium and alcuronium with propofol and thiopental].

UNLABELLED: Does propofol or thiopentone enhance the effect of nondepolarizing muscle relaxants? We evaluated the effects of propofol and thiopentone on the pharmacodynamics of atracurium and alcuronium in 43 surgical patients (ASA I and II) under general anaesthesia. METHODS: The patients were randomized into five groups, A-E. Anaesthesia was induced in all patients with fentanyl 4 micrograms/kg i.v. Patients in groups A and C patients received thiopentone 7 mg/kg i.v., and relaxation was achieved with alcuronium 0.25 mg/kg (group A) and atracurium 0.5 mg/kg (group C). Electromyography (train of four, TOF) was used to determine the time of onset of relaxation (AZ) and the maximum degree of blockade (T%). The recovery times to 25%, 50% and 75% of baseline muscle strength were recorded. Additionally, the TOF ratio T4:T1 was calculated, indicating the probable end of relaxation at a ratio of 0.7. At the beginning of the recovery phase (T1 = 15%) propofol 1% 3 mg/kg was given, and the effect on the TOF was measured. Patients in groups B and D patients received total intravenous anaesthesia (TIVA) with propofol 1% 6-12 mg/kg per hour continuously after induction with 3 mg/kg. The action profile of alcuronium 0.25 mg/kg (group B) and atracurium 0.5 mg/kg (group D) were recorded. Group E patients received thiopentone (10 mg/kg per hour) under the use of atracurium 0.5 mg/kg. Ventilation was performed with 30%/70% oxygen and N2O. The results were analyzed for significance using the Mann-Whitney U-test (P = 0.019). RESULTS: A slight difference in AZ was noted for alcuronium under the use of TIVA between propofol and thiopentone: 13 min and 5 min, respectively. Otherwise, the pharmacodynamics (T% and recovery of neuromuscular function) of the two relaxants exhibited no major differences related to thiopentone, propofol or their combination. The TOF was not influenced under additional propofol application. Noteworthy were the wide distribution of the time course of action (up to 3 h) and the magnitude of T% depression under alcuronium. CONCLUSION: Propofol and thiopentone have no potentiating influence on the time course of action and the magnitude of relaxation with alcuronium and atracurium. Pharmacodynamics of nondepolarizing muscle relaxants do not seem to be influenced by these two hypnotics.

Adjuvants, Anesthesia↗
PubMed1996

Opposite effects of alcuronium on agonist and on antagonist binding to muscarinic receptors.

Alcuronium is known to retard allosterically the dissociation of [3H]N-methylscopolamine from muscarinic M2 receptors, thereby augmenting the binding of this antagonist. Functionally, alcuronium behaves as a weak antimuscarinic agent and induces in combination with N-methylscopolamine an overadditive antimuscarinic action with oxotremorine-M as the agonist. The effect of alcuronium on the binding of [3H]oxotremorine-M was studied in porcine heart homogenates. Agonist binding was concentration dependently inhibited with a Ki = 0.48 +/- 0.03 microM (means +/- S.D., n = 3). Under identical conditions [3H]N-methylscopolamine binding was elevated. Alcuronium, 100 microM, which nearly prevented the dissociation of [3H]N-methylscopolamine, retarded the rate of dissociation of [3H]oxotremorine-M only by a factor of two. These findings support the notion that the overadditive antimuscarinic action of alcuronium in conjunction with N-methylscopolamine is based on a shift by alcuronium of the interplay between agonist and antagonist in favour of the antagonist.

Alcuronium↗
PubMedDate not supplied

Positive allosteric action of alcuronium on solubilized cardiac muscarinic receptors.

Alcuronium was found earlier to increase the binding of (3H)methyl-N-scopolamine [(3H)NMS] to muscarinic receptors in membranes of rat heart atria by increasing the receptors' affinity for (3H)NMS, without altering the number of (3H)NMS binding sites. We have now investigated how the interaction of alcuronium with muscarinic receptors is affected by solubilization. In experiments on pig heart atria, alcuronium had a positive allosteric effect on (3H)NMS binding both to unsolubilized receptors and to receptors solubilized by digitonin and deoxycholate. The cooperativity coefficient alpha was 0.39 +/- 0.01 for unsolubilized and 0.57 +/- 0.01 for solubilized receptors. Under the conditions used for solubilization, muscarinic receptors did not interact with G proteins, as indicated by experiments with the binding of carbachol in the absence and presence of a stable GTP analogue. Alcuronium slowed down the rates of (3H)NMS association with, and dissociation from, solubilized receptors; the dissociation rate constant was diminished more than 300 times by 30 microM alcuronium. The results show that the positive allosteric action of alcuronium on cardiac muscarinic receptors and its effect on the kinetics of radioligand binding are preserved after receptor solubilization and do not depend on the interaction of receptors with G proteins.

Alcuronium↗
PubMed2002

Evaluation of the impurity profile of alcuronium by means of capillary electrophoresis.

Alcuronium, a neuromuscular blocking drug, was recently introduced to the European Pharmacopoeia. A HPLC method is described to limit the impurities of alcuronium, namely the diallylcaracurine (DAC) and the allyl-Wieland-Gumlich-aldehyde (WCA), to less than 0.5%. Since alcuronium and all impurities are quaternary salts, capillary electrophoresis (CE) is highly suitable to evaluate the impurity profile. Using 12 mM heptakis-(2,6-di-O-methyl)-beta-cyclodextrin in a 50 mM phosphate buffer at pH 5.5 or 50 mM diethanolamine buffer (pH 9.2)-acetonitrile 19:1 containing heptakis-(2,3-O-diacetyl-6-sulfo)-beta-cyclodextrin the impurities could be baseline separated and quantified. The limit of detection for DAC and WCA was found to be in the same range as found with HPLC; thus, less than 0.1% of both DAC and WCA could be detected in the solution for injection in presence of alcuronium. In injection solutions of alcuronium which were stored at higher temperatures three additional, unidentified impurities were detected. In addition, the conversion of alcuronium to DAC, occurring under acidic condition, was monitored by means of the CE method developed.

Alcuronium↗
PubMed1985

[Course of the neuromuscular block under atracurium. Comparison with alcuronium].

Using a standardized anaesthetic protocol, the continuous monitoring of the twitch height after a 0.1 Hz stimulus was used to follow the evolution of curarization following injection of either atracurium (0.6 mg . kg-1) or alcuronium (0.2 mg . kg-1). The maximum twitch height inhibition was always greater than 99% of the control value and occurred after 107 +/- 50 s with atracurium (n = 30) and 172 +/- 120 s for alcuronium (n = 30) (p less than 0.02). Although surgical stage of muscular relaxation (twitch height less than 25% of reference value) was the same for both drugs (55 +/- 15 min for alcuronium versus 52 +/- 10 min for atracurium; n = 30 for both groups), the clinical duration (spontaneous restoration of twitch height to 90% of the reference value) was significantly longer (p less than 0.005) for alcuronium: 89 +/- 20 min (n = 10) versus 62 +/- 9 min for atracurium (n = 10). The spontaneous return to normal of the train of four was also significantly longer (p less than 0.001) for alcuronium: 118 +/- 23 min (n = 10) versus 69 +/- 7 min for atracurium (n = 10). The recovery index (the time required for twitch height to rise from 25% to 75%) was three times quicker (p less than 0.01) for atracurium (10 +/- 3 min; n = 10) than for alcuronium (30 +/- 13 min; n = 10).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1983

Alcuronium kinetics and plasma concentration-effect relationship.

The kinetics and dynamics of the neuromuscular blocker alcuronium were investigated in 12 surgical patients who received bolus and infusion regimens. In six patients the duration of the infusion was sufficiently long so that a steady-state alcuronium plasma concentration was reached (mean SD, 0.80 +/- 0.23 micrograms/ml). In the remaining six patients a steady state was not reached but the alcuronium concentration at the end of the infusion was 0.91 +/- 0.39 micrograms/ml. Alcuronium kinetic parameters did not differ between the two groups or from those obtained previously after bolus doses. In six patients for whom sufficient alcuronium concentration-time response data were available over the 0 to 100% response range, various mathematic models were used to characterize the concentration-effect relationship. A dynamic model incorporating a separate effect compartment connected to the central compartment was found to be the most appropriate. The (mean +/- SD) rate constant for equilibration of alcuronium concentration and effect was found to be 0.24 +/- 0.11 min-1, whereas the steady-state concentration required to induce 95% paralysis was 0.91 +/- 0.35 micrograms/ml (mean +/- SD).

Adolescent↗
PubMed1995

Alcuronium: a pharmacodynamic and pharmacokinetic update.

Alcuronium may be considered a muscle relaxant of historical rather than clinical significance. However, recent information from the manufacturer revealed its persisting clinical use in 26 countries worldwide. Thus, a pharmacodynamic-pharmacokinetic update appears mandatory. An intravenous (IV) single-bolus injection of alcuronium (0.25 mg/kg = ED95) was administered to 10 patients undergoing maxillofacial surgery during nitrous-oxide opioid anesthesia. Alcuronium neuromuscular block (evoked twitch tension), plasma concentration, and renal elimination (high-performance liquid chromatography [HPLC] assay) were measured during the 12-h after its administration. The time of onset, the time from end of injection to recovery to 25% of control twitch tension (DUR25%), and the recovery index were 2.2 +/- 1.2, 54 +/- 14, and 37 +/- 11 min, respectively (mean +/- SD). Two hours after the injection of alcuronium, partial recovery from the neuromuscular block had occurred from 100% to 26% +/- 24% depression of twitch tension, although less than 25% of the injected dose was recovered from the urine. The 12-h plasma concentration and urinary recovery were 0.1 +/- 0.08 mg/L (one-sixth of the 50% inhibitory concentration) and 61% +/- 20%, respectively. Recovery from neuromuscular block was dominated by intercompartmental distribution rather than by renal elimination. Since alcuronium does not undergo biodegradation, our data may serv as a reference for the complex pharmacokinetics of readily metabolized modern muscle relaxants. The long plasma half-life with slow excretion merits attention with respect to the erroneous original perception that alcuronium was an intermediate-acting muscle relaxant.

Adult↗
PubMed1983

Alcuronium kinetics in patients undergoing cardiopulmonary bypass surgery.

1 The disposition of alcuronium was investigated in 10 patients undergoing surgery involving cardiopulmonary bypass (CPB) and compared with results from a group of non-cardiac patients studied previously. 2 After intravenous administration of a combined bolus and infusion dosage regimen, plasma concentrations fell in a bi-exponential fashion to a mean value of 0.55 micrograms/ml immediately before the start of extracorporeal circulation. 3 During CPB an apparent steady-state of alcuronium was reached immediately after commencement of CPB, however plasma concentrations were some 50% higher than those noted prior to commencement of CPB and those predicted using previous pharmacokinetic data from normal surgical patients. 4 Once CPB was completed and the alcuronium infusion terminated, post-infusion alcuronium plasma concentrations again appeared to decline bi-exponentially with time. 5 Of the pharmacokinetic parameters which were calculated model-independently, the apparent volume of distribution (Vss) was unchanged (329 vs 313 ml/kg) and the elimination half-life (t1/2,z) (532 vs 199 min) was prolonged and the plasma clearance (CL) (0.8 vs 1.34 ml min-1kg-1) markedly reduced in these patients compared to non-cardiac surgical patients. 6 As a result of these changes in alcuronium concentration during CPB and the diminished elimination of alcuronium following CPB, a closer monitoring of neuromuscular function may be necessary in cardiac patients undergoing CPB.

Adult↗
PubMed1995

Potentiation by alcuronium of the antimuscarinic effect of N-methylscopolamine in guinea pig left atria.

Alcuronium is known to stabilize allosterically the binding of the muscarinic antagonist N-methylscopolamine to muscarinic M2 receptors and thus to elevate the equilibrium binding of N-methylscopolamine in homogenized cardiac tissue. In order to check for a functional consequence of this effect, the action of alcuronium alone and in combination with N-methylscopolamine was determined in contracting guinea pig left auricles with oxotremorine-M as the negative inotropic agonist. For sake of comparison, the allosteric modulator W84 = hexane-1,6-bis(dimethyl-3'- phthalimidopropyl-ammonium bromide) was included. Alcuronium displayed a weak antimuscarinic action (pA2 = 5.7). In conjunction with 10(-7) M N-methylscopolamine, alcuronium (> or = 10(-6) M) induced a more pronounced antimuscarinic effect than expected for a combination of competitive antagonists. The extent of overadditivity with combinations of W84 and 10(-7) M N-methylscopolamine was smaller. In conclusion, alcuronium potentiates the antimuscarinic effect of N-methylscopolamine in contracting cardiac preparations with high effectivity.

Alcuronium↗
PubMed1986

Evoked electromyographic and mechanical responses of the adductor pollicis compared during the onset of neuromuscular blockade by atracurium or alcuronium, and during antagonism by neostigmine.

The effects of atracurium and alcuronium on the evoked mechanical and electromyographic responses of the adductor pollicis were investigated in 30 adult patients. The ulnar nerve was stimulated with trains of four supramaximal pulses of 0.2 ms duration and a frequency of 2 Hz at intervals of 20 s. The mechanical response was measured using a strain gauge force transducer and the evoked compound action potential (ECAP) was recorded simultaneously using a Medelec MS91 electromyography system. Depression of the electromyographic and mechanical responses, caused by atracurium, was similar during onset and antagonism of blockade. During onset of blockade by alcuronium, the mechanical response was depressed to a significantly greater extent compared with the ECAP. This difference was not observed during antagonism with neostigmine. The rates of onset of atracurium and alcuronium were generally similar, but the rate of onset of mechanical fade was greater in the alcuronium group. There was no significant quantitative difference between the rates of antagonism of alcuronium and atracurium when assessed by the mechanical first response ratio. Electromyographic first response and electromyographic and mechanical train-of-four ratios recovered more rapidly in the atracurium group. These findings suggest that the differences between mechanical and electromyographic measurements of neuromuscular blockade are drug-specific and are more pronounced during the onset of blockade than during its antagonism by neostigmine.

Adult↗
PubMed1987

Recovery of respiration after neuromuscular blockade with alcuronium.

Alcuronium 0.2 mg kg-1 was given to six patients to investigate the simultaneous recovery of breathing and peripheral neuromuscular function. Anaesthesia was maintained with 66% nitrous oxide in oxygen supplemented with 0.5% halothane, and the patients were ventilated to normocarbia. Patients were disconnected from the ventilator after the reappearance of the tetanic response. This response returned at a mean time of 19.2 min after the injection of alcuronium and oxygenation was maintained thereafter by means of apnoeic diffusion. Spontaneous breathing returned at a mean time of 23.6 min after the injection of alcuronium. Sixty minutes after the administration of alcuronium, respiratory exchange was judged adequate, and at that time neuromuscular function was still markedly depressed with a tetanic height less than 25% of control. It was concluded that, because of the slow recovery of neuromuscular function, alcuronium should be reserved for the longer surgical procedure.

Adolescent↗
PubMed1988

Recovery of neuromuscular function and postoperative morbidity following blockade by atracurium, alcuronium and vecuronium.

Recovery of neuromuscular function and postoperative morbidity were studied in 51 fit female patients who had nonemergency gynaecological laparoscopy as inpatients. They were allocated randomly to one of three groups to receive either atracurium 0.31 mg/kg, alcuronium 0.25 mg/kg, or vecuronium 0.06 mg/kg as part of an otherwise standard anaesthetic technique. There were neither differences in intubation conditions nor in the occurrence of postoperative diplopia whichever muscle relaxant was used. Deficits in grip strength and expiratory force were seen at one hour after reversal with atropine 1.2 mg and neostigmine 2.5 mg in all patients, deficits which persisted for 3 hours in those who received alcuronium. The recovery of inspiratory force was slower and less complete at up to 3 hours in those who received alcuronium and there was a high incidence of minor postoperative morbidity at up to 24 hours in each of the three groups. The only statistical difference in symptomatic morbidity was an increase in muscle weakness in those who received alcuronium compared with atracurium at 3 hours after laparoscopy. Only 25%, 20% and 31% of the patients who received atracurium, alcuronium and vecuronium respectively said that they would have liked to be day stay patients.

Adult↗