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PubMedDate not supplied

Comparative effects of desflurane and isoflurane on vecuronium-induced neuromuscular blockade.

STUDY OBJECTIVE: To evaluate the neuromuscular effects of a nondepolarizing muscle relaxant (vecuronium) during anesthesia with equipotent concentrations of either desflurane or isoflurane. DESIGN: Randomized open study comparing effects of desflurane and isoflurane on vecuronium-induced neuromuscular blockade. SETTING: University-affiliated medical center. PATIENTS: Forty-five healthy adults undergoing elective surgical procedures randomly assigned to receive either desflurane, nitrous oxide (N2O), and vecuronium or isoflurane, N2O, and vecuronium for maintenance of general anesthesia. INTERVENTIONS: Following a standardized induction sequence, patients receiving either desflurane and N2O or isoflurane and N2O were administered bolus doses of vecuronium equal to 0.01, 0.02, or 0.03 mg/kg intravenously (IV) during the maintenance period. Neuromuscular transmission was measured using a Relaxograph monitor. MEASUREMENTS AND MAIN RESULTS: Vecuronium produced similar depression of neuromuscular function at equipotent (50% of the minimum alveolar concentration) end-tidal concentrations of isoflurane 0.6% and desflurane 3.0%. Following administration of vecuronium 0.01 to 0.03 mg/kg IV, onset times (3.4 +/- 0.4 minutes to 3.2 +/- 0.4 minutes and 3.2 +/- 0.5 minutes to 3.0 +/- 0.6 minutes), maximum T1 twitch depression (80% +/- 10% to 95% +/- 9% and 81% +/- 9% to 97% +/- 10%), clinical duration of blockade (12 +/- 5 minutes to 20 +/- 8 minutes and 10 +/- 5 minutes to 19 +/- 17 minutes), and T1 recovery times (10 +/- 3 minutes to 12 +/- 6 minutes and 10 +/- 3 minutes to 12 +/- 4 minutes) were similar in the isoflurane and desflurane treatment groups, respectively (means +/- SD). CONCLUSION: Vecuronium has similar neuromuscular effects when administered in the presence of desflurane 3% and isoflurane 0.6%.

Adult↗

PubMed1984

Vecuronium-induced neuromuscular blockade during enflurane, isoflurane, and halothane anesthesia in humans.

To determine the effect of the commonly used volatile anesthetics on a vecuronium-induced neuromuscular blockade, the authors studied 54 patients anesthetized with 1.2 MAC or 2.2 MAC enflurane, isoflurane, or halothane (MAC value includes contribution from 60% nitrous oxide). During 1.2 MAC enflurane, isoflurane, and halothane, the ED50S (the doses depressing twitch tension 50%) for vecuronium were 12.8, 14.7, and 16.9 micrograms/kg, respectively. During 2.2 MAC enflurane, isoflurane, and halothane, the ED50S for vecuronium were 6.3, 9.8, and 13.8 micrograms/kg, respectively (P less than 0.05). Time from injection to peak effect was the same for each anesthetic group (6.5 +/- 0.5 min, mean +/- SD), except for the group given 2.2 MAC enflurane (9.7 +/- 0.6 min) (P less than 0.05). The duration of a 50% block from injection to 90% recovery was the same for each group (mean 20 +/- 4 min), except for the group given 2.2 MAC enflurane (46.5 min) (P less than 0.05). The authors conclude that enflurane is the most potent volatile anesthetic, followed by isoflurane and then halothane, in augmenting a vecuronium-induced neuromuscular blockade. Increasing the concentration of volatile anesthetic has less effect on a neuromuscular blockade produced by vecuronium than on one produced by other nondepolarizing relaxants (e.g., pancuronium and d-tubucurarine).

Dose-Response Relationship, Drug↗

PubMedDate not supplied

Functional recovery after neuromuscular blockade in mechanically ventilated critically ill patients.

BACKGROUND: An estimated 24% to 70% of individuals have prolonged paralysis or severe weakness after receiving neuromuscular blocking agents (NMBAs) when therapy is terminated. OBJECTIVES: The purposes of this study were to (1) evaluate the relationship between recovery of neuromuscular transmission (NMT) and functional muscle activity after NMBA administration; (2) evaluate the relationship between delayed recovery of NMT or muscle activity and functional performance; and (3) determine the predictors of delayed recovery of NMT, muscle activity, and functional performance. METHODS: This was a multisite study using a prospective, nonexperimental, descriptive design with convenience sampling techniques. Instruments used included a five-point muscle score, Actigraph, and peripheral nerve stimulator. RESULTS: Key findings were as follows: (1) NMT returned promptly, whereas muscle activity remained severely depressed; (2) only two subjects (5%) recovered functional performance within 24 hours; (3) degree of muscle weakness immediately after neuromuscular blockade was associated with prolonged time to extubation and mobility; and (4) predictors of delayed recovery included cumulative dose of aminosteroid NMBAs, age, and renal function. CONCLUSION: Prolonged recovery of muscle activity and extreme weakness may occur despite brisk recovery of NMT after neuromuscular blockade.

Adult↗

PubMed2001

Effects of partial neuromuscular blockade on carotid baroreflex function during exercise in humans.

1. This investigation was designed to determine the contribution of central command to the resetting of the carotid baroreflex during static and dynamic exercise in humans. 2. Thirteen subjects performed 3.5 min of static one-legged exercise (20 % maximal voluntary contraction) and 7 min dynamic cycling (20 % maximal oxygen uptake) under two conditions: control (no intervention) and with partial neuromuscular blockade (to increase central command influence) using Norcuron (curare). Carotid baroreflex function was determined at rest and during steady-state exercise using a rapid neck pressure/neck suction technique. Whole-body Norcuron was repeatedly administered to effectively reduce hand-grip strength by approximately 50 % of control. 3. Partial neuromuscular blockade increased heart rate, mean arterial pressure, perceived exertion, lactate concentration and plasma noradrenaline concentration during both static and dynamic exercise when compared to control (P < 0.05). No effect was seen at rest. Carotid baroreflex resetting was augmented from control static and dynamic exercise by partial neuromuscular blockade without alterations in gain (P < 0.05). In addition, the operating point of the reflex was relocated away from the centring point (i.e. closer to threshold) during exercise by partial neuromuscular blockade (P < 0.05). 4. These findings suggest that central command actively resets the carotid baroreflex during dynamic and static exercise.

Adult↗

PubMed1993

Diabetic rats show more resistance to neuromuscular blockade induced by aminoglycoside antibiotics.

1. Neuromuscular blocking effect of gentamicin and neomycin evaluated in phrenic-nerve hemidiaphragm preparation in normal and diabetic rats and IC50 of both drugs determined from LDR curves. 2. IC50 of gentamicin was 0.91 +/- 0.05 and 1.67 +/- 0.08 mmol.l-1 for normal and diabetic rats respectively. 3. IC50 of neomycin was 0.42 +/- 0.02 and 0.61 +/- 0.06 mmol.l-1 for normal and diabetic rats respectively. 4. The results show diabetic rats are more resistant to neuromuscular blocking action of aminoglycoside antibiotics (AGs). 5. Replacement of sodium by lithium (1.5 and 5 mmol.l-1) in the media, reduced this effect of aminoglycosides (AGs) significantly. 6. It appears that the prevention of AGs induced-neuromuscular blockade by lithium is not significantly different in both groups.

Animals↗

PubMed1998

Comparison of acceleromyography and electromyography in vecuronium-induced neuromuscular blockade with xenon or sevoflurane anesthesia.

STUDY OBJECTIVES: To compare acceleromyography (AMG) and electromyography (EMG) with xenon or sevoflurane anesthesia during vecuronium-induced neuromuscular blockade. DESIGN: Prospective randomized study. SETTING: University hospital. PATIENTS: 28 ASA physical status I and II adult patients presenting for elective surgery. INTERVENTIONS: Patients received vecuronium for neuromuscular blockade and either xenon (n = 11) or sevoflurane (n = 17) anesthesia. MEASUREMENTS AND MAIN RESULTS: The first twitch depression, which was expressed as a ratio of the first twitch to that obtained before the blocking drug was administered (T1/Tc), was measured simultaneously by AMG and EMG. T1/Tc as measured by AMG consistently demonstrated greater depression than that by EMG during recovery. The limits of agreement were unacceptably wide, suggesting that T1/Tc obtained by AMG is a poor predictor of T1/Tc as measured by EMG. Such relations were not affected by the anesthetic (xenon or sevoflurane) used. CONCLUSION: AMG and EMG-cannot be used interchangeably with either xenon or sevoflurane anesthesia.

Acceleration↗

PubMed2002

[Pretreatment with lidocaine accelerates onset of vecuronium-induced neuromuscular blockade].

The purpose of this study was to investigate the effect of pre-treatment with lidocaine on the onset of vecuronium-induced neuromuscular block in a randomized, double-blinded trial. Thirty-one patients were randomly allocated to one of two groups according to the agents administrated 3 min prior to vecuronium injection; Group C, normal saline 0.75 ml.kg-1 and Group L, 2% lidocaine 1.5 mg.kg-1. Anesthesia was induced with propofol 1.5 mg.kg-1 followed by continuous infusion at 8 mg.kg-1.hr-1. Neuromuscular blockade was evaluated with accelerometry, which measured a train-of-four (TOF) pattern of abductor policies muscle. The disappearance of the first response in TOF was regarded as onset of neuromuscular block. Changes in systolic and diastolic arterial pressure (SBP, DBP) and heart rate (HR) were measured before and after tracheal intubation. Times to onset of neuromuscular blockade induced by vecuronium in Group L and Group C were 115 +/- 20 sec and 174 +/- 45 sec, respectively. After tracheal intubation, SBP, DBP and HR in both groups increased compared with those before tracheal intubation, but the changes were not significant. Changes in SBP, DBP and HR did not differ between Group L and Group C. The mechanisms by which lidocaine reduced the time to onset of neuromuscular block caused by vecuronium could not be clarified from our study, but this may be related to pre- and post-junctional effects of lidocaine at neuromuscular junction. In conclusion, administration of lidocaine prior to tracheal intubation reduces the time to onset of neuromuscular block caused by vecuronium, but does not attenuate changes in blood pressure and heart rate caused by tracheal intubation.

Adolescent↗

PubMed1992

Double burst stimulation for monitoring profound neuromuscular blockade: a comparison with posttetanic count and train of four.

Double burst stimulation (DBS) is a new nerve stimulation pattern introduced to facilitate tactile evaluation of recovery from neuromuscular blockade. DBS consists of two bursts of high frequency stimulations separated by a short time interval. The relationships between DBS, post-tetanic count (PTC) and train-of-four (TOF) on the evoked twitch response was investigated in 16 surgical patients and 7 intensive care patients given atracurium for muscle relaxation. A significant correlation between the twitch height of the first response to DBS and the number of post-tetanic responses was demonstrated when PTC was more than five (r = 0.47, p < 0.0003). When the first twitch of TOF was still not measurable, the first twitch of DBS ranged from 0 to 20% of the TOF-control twitch height. Furthermore the DBS ratio was significantly correlated to the TOF ratio (r = 0.92-0.96, p < 0.0002). It is concluded that DBS not only can be used for monitoring of recovery from neuromuscular blockade, but also for monitoring of intense degrees of neuromuscular blockade.

Electric Stimulation↗

PubMed1997

Incidence of awareness in total i.v. anaesthesia based on propofol, alfentanil and neuromuscular blockade.

BACKGROUND: There is no reliable technique for monitoring drug concentrations in total i.v. anaesthesia (TIVA) with muscle relaxation. An increased risk of awareness with TIVA has been stated as a possible drawback. The present study was conducted in order to assess the incidence of conscious awareness in TIVA based on propofol, alfentanil and neuromuscular blockade. METHODS: One thousand patients anaesthetized with TIVA based on propofol, alfentanil, and neuromuscular blockade were subjected postoperatively to a structured interview for conscious awareness on two separate occasions: on discharge from the post-anaesthesia care unit, and the day after anaesthesia. Five hundred of these patients were also interviewed a third time, approximately 1 week later. RESULTS: Two cases of awareness were detected (0.2%). One of these was identified immediately after extubation. The second patient had no memory of intraoperative events or dreams at the first interview, recalled a bad dream on the day after, and had explicit recall of intraoperative events at the interview 8 days later. In both cases, haemodynamic signs of inadequate anaesthesia were present. The incidence of conscious awareness in this study is similar to the lowest previously reported incidence of awareness following general anaesthesia in patients who had been paralyzed and thereafter subjected to a structured postanesthesia interview. CONCLUSIONS: If the true incidence of conscious awareness is to be determined, interviews must be extended beyond the first postoperative day. Our study indicates that if appropriate dosing of propofol and alfentanil are adhered to, and proper action is taken in case of haemodynamic alterations suggestive of inadequate anaesthesia, the incidence of conscious awareness in non-cardiac TIVA with neuromuscular blockade is low.

Adolescent↗

PubMed1995

Monitoring neuromuscular blockade in the adult ICU.

Although neuromuscular blocking agents are now administered in intensive care units for extended periods, no standard has been established for their use in critically ill patients. Also, despite wide variations in individual response to neuromuscular blockade, the level of paralysis is not monitored consistently. Paralytic agents are associated with numerous side effects such as prolonged weakness, which is gaining widespread attention. Side effects may be minimized or prevented by consistent and precise monitoring of the degree of blockade. Monitoring is best accomplished by the expert use of the peripheral nerve stimulator. The evoked responses must be correlated with clinical signs of muscle movement. Furthermore, staff education regarding the pharmacology of these agents and the proper operation of the peripheral nerve stimulator must be ongoing.

Electric Stimulation↗

PubMed1989

Cell death of motoneurons in the chick embryo spinal cord. XI. Acetylcholine receptors and synaptogenesis in skeletal muscle following the reduction of motoneuron death by neuromuscular blockade.

Treatment of chick embryos with neuromuscular blocking agents such as curare during periods of naturally occurring motoneuron death results in a striking reduction of this normal cell loss. Inactivity-induced changes in motoneuron survival were found to be associated with increased levels of AChRs and AChR-clusters in skeletal muscle and with increased focal sites of AChE that are innervated ('synaptic sites'). Treatment of embryos with curare after the normal cell death period (E12-E15) resulted in no change in motoneuron survival. Although AChR-clusters and focal sites of AChE were increased in these embryos on E16, many of these sites were uninnervated. Treatment of embryos with nicotine or decamethonium (E6-E10) also reduced neuromuscular activity but did not alter motoneuron survival nor did such treatment alter AChRs. The different effects of curare vs nicotine and decamethoniam on motoneuron survival and AChRs may be related to the fact that the former is a competitive blocker whereas the latter two drugs are depolarizing blockers. Finally, treatment of embryos (E6-9) with doses of curare (1 mg daily) that allow for the almost complete recovery of neuromuscular activity a few days following treatment (by E16) resulted in the gradual loss of the excess motoneurons that were present on E10, and by E16 the number of remaining AChR clusters and focal sites of AChE were also decreased to levels comparable to control values. Inactivity-induced changes in AChRs or AChR-clusters may be an important factor in the reduced motoneuron death that accompanies neuromuscular blockade during critical stages of development. These receptor changes very likely reflect increased synaptogenesis in the muscles of paralyzed embryos which in turn may act to reduce motoneuron death by providing increased access to muscle-derived neurotrophic molecules.

Animals↗

PubMed1991

Is the diagnosis of significant residual neuromuscular blockade improved by using double-burst nerve stimulation?

This study evaluated the use of double-burst stimulation (DBS) in the diagnosis of significant post-operative residual neuromuscular blockade. Ninety patients were allocated to three equal groups. In Group A the degree of residual neuromuscular blockade was assessed by clinical criteria (CC) only; in Group B by CC and manual evaluation of the response to train-of-four (TOF) nerve stimulation; and in Group C by CC, manual evaluation of the response to TOF, and DBS stimulation. Immediately after arrival in the recovery room mechanical twitch was recorded using TOF stimulation. The mean (+/- SD) TOF ratios were 0.53 +/- 0.19 in Group A, 0.67 +/- 0.11 in Group B and 0.81 +/- 0.08 in Group C. The incidence of a TOF ratio of less than 0.7 was 83.3% in Group A, 56.7% in Group B and 6.7% in Group C. It is concluded that the use of DBS enabled the anaesthetist to recognize significant residual block and thus reduced the incidence of post-operative residual neuromuscular blockade.

Analysis of Variance↗

PubMed2001

Neuromuscular blockade in the intensive care unit.

Neuromuscular blocking agents (NMBA) are frequently utilized in the ICU, primarily to facilitate mechanical ventilation. An ideal NMBA is nondepolarizing, has no propensity to accumulate, is easily titrated, has a rapid onset and offset, does not rely on organ function for metabolism, and has no toxic or active metabolites. Current NMBAs are classified as aminosteroids or benzylisoquinoliniums and have different features, but none are ideal. Selection of the best NMBA is determined by individual patient characteristics. Proper use of these agents includes a comprehensive plan to manage all aspects of care affected by NMBA, as well as monitoring of clinical effect and degree of neuromuscular blockade via periodic peripheral nerve stimulation. There are well-recognized complications of NMBA, including prolonged drug effect and acute quadriplegic myopathy. The latter condition can result in prolonged rehabilitation. The use of an NMBA can be essential for the successful outcome from critical illness; however, cautious use of these agents with a structured approach to minimize complications is urged.

Journal Article↗

PubMed1999

The effects of dexmedetomidine on neuromuscular blockade in human volunteers.

UNLABELLED: The neuromuscular effects of dexmedetomidine in humans are unknown. We evaluated the effect of dexmedetomidine on neuromuscular block and hemodynamics during propofol/alfentanil anesthesia. During propofol/alfentanil anesthesia, the rocuronium infusion rate was adjusted in 10 volunteers to maintain a stable first response (T1) in the train-of-four sequence at 50% +/- 3% of the pre-rocuronium value. Dexmedetomidine was then administered by computer-controlled infusion, targeting a plasma dexmedetomidine concentration of 0.6 ng/mL for 45 min. The evoked mechanical responses of the adductor pollicis responses (T1 response and T4/T1 ratio), systolic blood pressure (SBP), heart rate (HR), and transmitted light through a fingertip were measured during the dexmedetomidine infusion and compared with predexmedetomidine values using repeated-measures analysis of variance and Dunnett's test. Plasma dexmedetomidine levels ranged from 0.68 to 1.24 ng/mL. T1 values decreased during the infusion, from 51% +/- 2% to 44% +/- 9% (P < 0.0001). T4/T1 values did not change during the infusion. Plasma rocuronium concentrations increased during the infusion (P = 0.02). Dexmedetomidine increased SBP (P < 0.001) and decreased HR (P < 0.001) (5-min median values) during the infusion compared with values before the infusion. Dexmedetomidine increased the transmitted light through the fingertip by up to 41% +/- 8% during the dexmedetomidine infusion (P < 0.001).We demonstrated that dexmedetomidine (0.98 +/- 0.01 microg/kg) increased the plasma rocuronium concentration, decreased T1, increased SBP, and decreased finger blood flow during propofol/alfentanil anesthesia. We conclude that dexmedetomidine-induced vasoconstriction may alter the pharmacokinetics of rocuronium. IMPLICATIONS: We studied the effect of an alpha2-agonist (dexmedetomidine) on rocuronium-induced neuromuscular block during propofol/alfentanil anesthesia. We found that the rocuronium concentration increased and the T1 response decreased during the dexmedetomidine administration. Although these effects were statistically significant, it is unlikely that they are of clinical significance.

Adrenergic alpha-Agonists↗

PubMedDate not supplied

Interactions of nifedipine and diltiazem with muscle relaxants and reversal of neuromuscular blockade with edrophonium and neostigmine.

The effects and interactions of nifedipine and diltiazem with tubocurarine, gallamine and pancuronium and their reversal by edrophonium and neostigmine were studied on isolated skeletal muscle of the chick. The nerve-muscle preparation of the chick biventer cervicis was set up in an organ bath containing Krebs-Henseleit solution and the mechanical responses produced either by motor nerve stimulation or by drug application were recorded isometrically. The results showed that nifedipine (29-1015 microM) and diltiazem (22-572 microM) reduced, in a dose-dependent manner, the amplitude of indirectly-elicited twitch tension, evoked at 0.2 Hz with 5-10 V and 0.2 msec pulse duration, and increased the neuromuscular blockade produced by d-tubocurarine (1-254 microM), gallamine (0.01-2.0 microM) and pancuronium (0.01-7.0 microM). Edrophonium (250 nM) and neostigmine (150 nM) completely reversed the neuromuscular blockade produced by the muscle relaxants, alone and in combination with nifedipine or diltiazem. The mean IC50 values (concentrations to produce 50% of maximum inhibition) of nifedipine and diltiazem-induced depression of twitch response were 324 +/- 16 microM and 143 +/- 11 microM respectively (means +/- S.E., n = 6). Nifedipine, in high concentrations, produced small contractions (0.4 +/- 0.1 g of tension, n = 6), in the chick muscle. In contrast, diltiazem produced no such contractions in the muscle. However, in concentrations which had little effect on twitch response, diltiazem (20 microM) and nifedipine (50 microM) both increased the neuromuscular blockade produced by tubocurarine, gallamine and pancuronium by about 2-fold. Increasing the external calcium concentration, by a 2-fold, did not reverse or antagonize the inhibitory effects of diltiazem or nifedipine. It was concluded that diltiazem and nifedipine inhibit indirectly-elicited twitch tension and intensify neuromuscular blockade produced by muscle relaxants. These effects of nifedipine and diltiazem may be due to blocking influx of calcium and on release of acetylcholine from presynaptic nerve terminals.

Animals↗

PubMed1989

Neuromuscular blockade induced by flunarizine alone and in combination with pancuronium, suxamethonium or neomycin: studies in isolated rat phrenic-hemidiaphragm preparations.

The in vitro effects of flunarizine on indirectly- and directly-elicited contractions in rat phrenic-hemidiaphragm preparations were studied. The interactions of flunarizine with non-depolarizing and depolarizing neuromuscular blocking drugs (pancuronium and suxamethonium) and with an aminoglycoside antibiotic (neomycin) were also evaluated. Flunarizine induced a slowly developing concentration-dependent reduction of indirectly-elicited diaphragm twitch height, but only slightly reduced directly-elicited contractions. Flunarizine 1 and 5 mumol.l-1 produced a concentration-dependent enhancement of pancuronium-induced neuromuscular blockade, whereas suxamethonium blockade was significantly increased by flunarizine 5 mumols.l.-1 only. Moreover, both flunarizine 1 and 5 mumols.l-1 also increased the neuromuscular blockade induced by neomycin. In conclusion, flunarizine induced neuromuscular blockade and enhanced the effects of several neuromuscular blocking agents to varying degrees in vitro.

Animals↗

PubMed1989

A contribution to the monitoring of neuromuscular blockade: an evaluation of the Datex Relaxograph.

The Datex Relaxograph is a neuromuscular transmission monitor, which measures the degree of neuromuscular blockade during anesthesia. In order to evaluate the reliability of the Relaxograph, results, obtained with this apparatus, were compared with simultaneous mechanical measurements obtained with the Myograph 2000 (Biometer). Although there was a good correlation between the two throughout the study, a shift towards mechanical responses was observed in all cases. Subsequently, the Relaxograph was used to evaluate atracurium and vecuronium when given accordingly to the priming principle. Results show that neither drug offers major clinical advantages over the other. In a third study, a new bolus-constant infusion regimen of atracurium was evaluated. Results show that it produces a predictable and stable neuromuscular blockade.

Adult↗

PubMed1987

Glycopyrrolate intensifies neuromuscular blockade produced by atracurium in the rat diaphragm preparation.

The effect of glycopyrrolate (Glycopyrronium, a muscarinic antagonist) (10 mumol.litre-1) and neostigmine (1 mumol.litre-1) on atracurium (0.1-100 mumol.litre-1) - induced neuromuscular blockade was studied in the rat isolated phrenic nerve-diaphragm preparation, to see if glycopyrrolate intensified the neuromuscular blockade produced by atracurium in this preparation. Atracurium had a rapid onset of blockade, reaching a complete block in 30-40 s. Glycopyrrolate had no significant effect on indirectly-elicited twitch (0.2 Hz) tension, whereas it significantly increased atracurium-induced depression of twitch tension and shortened the time needed to a complete block by 10 s. Combinations of glycopyrrolate+ neostigmine, only slightly reversed atracurium-induced blockade, if compared to the reversal by neostigmine alone. The mean concentrations to produce 50% depression of twitch tension were: 1.6 +/- 0.1 (atracurium), 0.3 +/- 0.1 (atracurium +glycopyrrolate), 4.8 +/- 0.2 (atracurium +neostigmine) and 2.7 +/- 0.1 mumol.litre-1 (atracurium +glycopyrrolate +neostigmine) (means +/- SEM, n = 6, P less than 0.001, with respect to control value of atracurium alone). It was concluded that glycopyrrolate enhanced atracurium-induced neuromuscular blockade in the rat diaphragm preparation, and that this effect should be noted when dosing glycopyrrolate in man.

Animals↗