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Journal articles on the topic 'Vecuronium'

Author: Grafiati

Published: 4 June 2021

Last updated: 3 February 2022

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1

Wright, Peter M. C., Paul Hart, Marie Lau, Ronald Brown, Manohar L. Sharma, Larry Gruenke, and Dennis M. Fisher. "The Magnitude and Time Course of Vecuronium Potentiation by Desflurane Versus Isoflurane." Anesthesiology 82, no. 2 (February 1, 1995): 404–11. http://dx.doi.org/10.1097/00000542-199502000-00011.

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Background Preliminary studies suggest that desflurane and isoflurane potentiate the action of muscle relaxants equally. However, variability between subjects may confound these comparisons. A crossover study was performed in volunteers on the ability of desflurane and isoflurane to potentiate the neuromuscular effect of vecuronium, to influence its duration of action, and on the magnitude and time course of reversal of potentiation when anesthesia was withdrawn. Methods Adductor pollicis twitch tension was monitored in 16 volunteers given 1.25 MAC desflurane on one occasion, and 1.25 MAC isoflurane on another. In eight subjects, vecuronium bolus dose potency was determined using a two-dose dose-response technique; the vecuronium infusion dose requirement to achieve 85% twitch depression also was determined. Also in these subjects, the magnitude and time course of spontaneous neuromuscular recovery were determined when the anesthetic was withdrawn while maintaining a constant vecuronium infusion. In the other eight subjects, the time course of action of 100 micrograms/kg vecuronium was determined. Results Vecuronium's ED50 and infusion requirement to maintain 85% twitch depression were 20% less during desflurane, compared to isoflurane, anesthesia; vecuronium plasma clearance was similar during the two anesthetics. After 100 micrograms/kg vecuronium, onset was faster and recovery was longer during desflurane anesthesia. When the end-tidal anesthetic concentration was abruptly reduced from 1.25 to 0.75 MAC, twitch tension increased similarly (approximately 15% of control), and time for the twitch tension to reach 90% of the final change was similar (approximately 30 min) with both anesthetics. Decreasing anesthetic concentration from 0.75 to 0.25 MAC increased twitch tension by 46 +/- 10% and 25 +/- 7% of control (mean +/- SD, P < 0.001) with desflurane and isoflurane, respectively; 90% response times for these changes were 31 +/- 10 min and 18 +/- 7 min (P < 0.05), respectively. Conclusions Desflurane potentiates the effect of vecuronium approximately 20% more than does an equipotent dose of isoflurane.

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2

Fisher, Dennis M., Janos Szenohradszky, Peter M. C. Wright, Marie Lau, Ronald Brown, and Manohar Sharma. "Pharmacodynamic Modeling of Vecuronium-induced Twitch Depression." Anesthesiology 86, no. 3 (March 1, 1997): 558–66. http://dx.doi.org/10.1097/00000542-199703000-00007.

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Background After bolus doses of nondepolarizing muscle relaxants, the adductor pollicis recovers from paralysis more slowly than the diaphragm and the laryngeal adductors, suggesting that the adductor pollicis is more sensitive than the respiratory muscles to effects of those drugs. In contrast, during onset, the respiratory muscles are paralyzed more rapidly than the adductor pollicis, suggesting that the respiratory muscles are more sensitive than the adductor pollicis. To reconcile these apparently conflicting findings, we determined vecuronium's pharmacokinetics and its pharmacodynamics at both the adductor pollicis and the laryngeal adductors. Methods Six volunteers were studied on two occasions during anesthesia with propofol. Mechanical responses to train-of-four stimulation were measured at the adductor pollicis and at the laryngeal adductors. Vecuronium (15-60 micrograms/kg) was given and arterial plasma samples were obtained from 0.5-60 min. Vecuronium doses differed by twofold on the two occasions. A pharmacokinetic model accounting for the presence and potency of vecuronium's 3-desacetyl metabolite and a sigmoid e-max pharmacodynamic model were fit to the resulting plasma concentration and effect (adductor pollicis and laryngeal adductors) data to determine relative sensitivities and rates of equilibration between plasma and effect site concentrations. Results The steady-state plasma concentration depressing laryngeal adductor twitch tension by 50% was approximately 1.5 times larger than that for the adductor pollicis. The equilibration rate constant between plasma and laryngeal adductor concentrations was about 1.5 faster than that between plasma and adductor pollicis concentrations. The Hill factor (gamma) that describes the steepness of the laryngeal adductor concentration-effect relation was approximately 0.6 times that of the adductor pollicis. Conclusions More rapid equilibration between plasma and laryngeal adductor vecuronium concentrations explains why onset is more rapid at the laryngeal adductors than at the adductor pollicis. During recovery, both rapid equilibration and lesser sensitivity of the laryngeal adductors contribute to earlier recovery.

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3

Stirt, Joseph A., William Maggio, Charles Haworth, Michael D. Minton, and Robert F. Bedford. "Vecuronium." Anesthesiology 67, no. 4 (October 1, 1987): 570–72. http://dx.doi.org/10.1097/00000542-198710000-00022.

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4

Wright, Peter M. C., Gerald McCarthy, Janos Szenohradszky, Manohar L. Sharma, and James E. Caldwell. "Influence of Chronic Phenytoin Administration on the Pharmacokinetics and Pharmacodynamics of Vecuronium." Anesthesiology 100, no. 3 (March 1, 2004): 626–33. http://dx.doi.org/10.1097/00000542-200403000-00024.

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Background The duration of action of vecuronium is reduced in patients receiving phenytoin. In this study, the authors examined, simultaneously, the influence of phenytoin on both the pharmacokinetics and the pharmacodynamics of vecuronium. Methods This study was approved by the institutional review board of the University of California, San Francisco, and patients gave written informed consent. Twenty-two patients, 11 taking phenytoin and all scheduled to undergo prolonged neurosurgical procedures with general anesthesia, participated in the study. In 12 patients (6 phenytoin, 6 control), vecuronium was infused at 7.5 microg x kg(-1) x min(-1) until the first response (T1) of each train-of-four decreased by 50%; in the remaining 10 patients (5 phenytoin, 5 control), 200 microg/kg vecuronium was infused over 10 min. Arterial blood samples were drawn at intervals over the next 5-7 h. Plasma concentrations of vecuronium and 3-desacetylvecuronium were measured by capillary gas chromatography. Pharmacokinetic and pharmacodynamic modeling was used to characterize the disposition of vecuronium and patient responses to it in the two groups. Results Clearance was typically increased by 138% (95% confidence interval, 93-183%) in patients taking phenytoin. The effect of vecuronium was well described using a sigmoid Emax model. The concentration of vecuronium giving 50% twitch depression was increased 124% (45-202%) in patients taking phenytoin. Conclusions Chronic phenytoin therapy reduces the effect of vecuronium by mechanisms that include both increased vecuronium metabolism and reduced sensitivity of the patient to circulating concentrations of vecuronium.

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5

Blobner, Manfred, Eberhard Kochs, Heidrun Fink, Barbara Mayer, Andreas Veihelmann, Thomas Brill, and Josef Stadler. "Pharmacokinetics and Pharmacodynamics of Vecuronium in Rats with Systemic Inflammatory Response Syndrome." Anesthesiology 91, no. 4 (October 1, 1999): 999. http://dx.doi.org/10.1097/00000542-199910000-00020.

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Background Insufficient detoxification caused by nitric oxide-related inhibition of cytochrome P450 may be important for metabolism of numerous drugs, including vecuronium. The present study investigated the pharmacodynamics and pharmacokinetics of vecuronium in rats with inflammatory liver dysfunction. Methods Male Sprague-Dawley rats (n = 56) were randomly allocated into two groups: In the sepsis group, liver inflammation was established by injection of 56 mg/kg heat-killed Corynebacterium parvum; control rats received the solvent. At day 4, groups were subdivided according to treatment with the nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine (250 mg/kg) or placebo. The aminopyrine breath test was performed to assess cytochrome P450 activity. Rats were anesthetized with propofol and mechanically ventilated. Duration of action of vecuronium (1.2 mg/kg) was measured by evoked mechanomyography (stimulation of the sciatic nerve, contraction of the gastrocnemius muscle). In seven rats of each subgroup a 50% neuromuscular blockade was established by a continuous vecuronium infusion. Vecuronium plasma levels were measured and plasma clearance of vecuronium was calculated. Nitric oxide synthesis was assessed by measuring nitrite/nitrate serum levels. Results In sepsis/placebo rats, vecuronium-induced neuromuscular blockade was prolonged (144% of contro/placebo), vecuronium plasma levels at 50% neuromuscular blockade were increased (122% of control/placebo), and plasma clearance was decreased (68% of control/placebo). N(G)-monomethyl-L-arginine therapy in rats with sepsis improved cytochrome P450 activity and plasma clearance of vecuronium, shortened duration of action of vecuronium, but did not alter the elevated vecuronium plasma levels. Conclusions A systemic inflammatory response syndrome with liver dysfunction results in decreased sensitivity to and a decreased elimination of vecuronium. Modulation of nitric oxide synthesis may be a strategy that can be used in the future to improve xenobiotic metabolism in sepsis.

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6

&NA;. "Vecuronium bromide see Fentanyl/halothane/vecuronium bromide." Reactions Weekly &NA;, no. 367 (September 1991): 12. http://dx.doi.org/10.2165/00128415-199103670-00063.

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7

Beaufort, Ton M., Johannes H. Proost, Jan-Gerard Maring, Emiel R. Scheffer, J. Mark K. H. Wierda, and Dirk K. F. Meijer. "Effect of Hypothermia on the Hepatic Uptake and Biliary Excretion of Vecuronium in the Isolated Perfused Rat Liver." Anesthesiology 94, no. 2 (February 1, 2001): 270–79. http://dx.doi.org/10.1097/00000542-200102000-00017.

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Background Hypothermia prolongs the time course of action of nondepolarizing muscle relaxants. It is not known whether this prolongation is caused by a reduced rate of extrahepatic distribution or elimination, liver uptake, metabolic clearance, or biliary excretion. Therefore, the authors studied the effects of hypothermia on the net hepatic uptake, metabolism, and biliary excretion of vecuronium in isolated perfused rat liver. Methods Livers of Wistar rats were perfused with Krebs Ringer solution (1% albumin, 3.3% carbon dioxide in oxygen, pH 7.36-7.42, 38 degrees C). Each perfusion experiment (recirculatory perfusion system) was divided into three phases. In phase 1, a bolus dose of vecuronium (950 microg) was followed by a continuous infusion of vecuronium (63 microg/min) throughout the perfusion experiment. In phase 2, the temperature was reduced to 28 degrees C. In phase 3, temperature was restored. In controls, the temperature was kept constant throughout the perfusion. Concentrations of vecuronium and its metabolites were measured in perfusion medium, bile, and liver homogenate. Parameters of a multicompartmental liver model were fitted to the concentration patterns in perfusion medium and in bile. Results Hypothermia increased vecuronium concentrations in the perfusion medium from 4.0 microg/ml (range, 2.5-6.6) to 15.6 microg/ml (11.5-18.4 microg/ml; P = 0.018). Hypothermia reduced the biliary excretion rate of 3-desacetyl vecuronium from 18% (range, 6-37%) to 16% (range, 4-19%) of that of vecuronium (P = 0.018). Pharmacokinetic analysis confirmed that hypothermia reduced the rate constants of hepatic uptake and metabolism from 0.219 to 0.053 and from 0.059 to 0.030, respectively. Conclusions Hypothermia significantly and reversibly reduced the net hepatic uptake of vecuronium. Hypothermia reduced the metabolism of vecuronium and the biliary excretion rate of 3-desacetyl vecuronium.

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8

&NA;. "Vecuronium bromide." Reactions Weekly &NA;, no. 1016 (August 2004): 18. http://dx.doi.org/10.2165/00128415-200410160-00061.

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&NA;. "Vecuronium bromide." Reactions Weekly &NA;, no. 299 (May 1990): 11. http://dx.doi.org/10.2165/00128415-199002990-00054.

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&NA;. "Vecuronium bromide." Reactions Weekly &NA;, no. 300 (May 1990): 12. http://dx.doi.org/10.2165/00128415-199003000-00049.

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&NA;. "Vecuronium bromide." Reactions Weekly &NA;, no. 304 (June 1990): 12. http://dx.doi.org/10.2165/00128415-199003040-00052.

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&NA;. "Vecuronium bromide." Reactions Weekly &NA;, no. 331 (December 1990): 11. http://dx.doi.org/10.2165/00128415-199003310-00061.

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&NA;. "Vecuronium bromide." Reactions Weekly &NA;, no. 332 (December 1990): 8. http://dx.doi.org/10.2165/00128415-199003320-00043.

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&NA;. "Vecuronium bromide." Reactions Weekly &NA;, no. 336 (January 1991): 8. http://dx.doi.org/10.2165/00128415-199103360-00039.

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&NA;. "Vecuronium bromide." Reactions Weekly &NA;, no. 599 (May 1996): 11. http://dx.doi.org/10.2165/00128415-199605990-00039.

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&NA;. "Vecuronium bromide." Reactions Weekly &NA;, no. 507 (June 1994): 16. http://dx.doi.org/10.2165/00128415-199405070-00080.

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&NA;. "Vecuronium bromide." Reactions Weekly &NA;, no. 621 (October 1996): 12. http://dx.doi.org/10.2165/00128415-199606210-00039.

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&NA;. "Vecuronium bromide." Reactions Weekly &NA;, no. 1370 (September 2011): 37. http://dx.doi.org/10.2165/00128415-201113700-00129.

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&NA;. "Vecuronium bromide." Reactions Weekly &NA;, no. 1191 (March 2008): 25. http://dx.doi.org/10.2165/00128415-200811910-00081.

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&NA;. "Vecuronium bromide." Reactions Weekly &NA;, no. 1420 (September 2012): 50. http://dx.doi.org/10.2165/00128415-201214200-00173.

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&NA;. "Vecuronium bromide." Reactions Weekly &NA;, no. 1429 (November 2012): 44. http://dx.doi.org/10.2165/00128415-201214290-00168.

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&NA;. "Vecuronium bromide." Reactions Weekly &NA;, no. 395 (April 1992): 12. http://dx.doi.org/10.2165/00128415-199203950-00057.

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&NA;. "Vecuronium bromide." Reactions Weekly &NA;, no. 371 (October 1991): 12. http://dx.doi.org/10.2165/00128415-199103710-00065.

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&NA;. "Vecuronium bromide." Reactions Weekly &NA;, no. 416 (August 1992): 12. http://dx.doi.org/10.2165/00128415-199204160-00055.

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&NA;. "Vecuronium bromide." Reactions Weekly &NA;, no. 421 (October 1992): 12. http://dx.doi.org/10.2165/00128415-199204210-00057.

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26

&NA;. "Vecuronium bromide." Reactions Weekly &NA;, no. 408 (July 1992): 12. http://dx.doi.org/10.2165/00128415-199204080-00050.

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27

&NA;. "Vecuronium bromide." Reactions Weekly &NA;, no. 1389 (February 2012): 42. http://dx.doi.org/10.2165/00128415-201213890-00154.

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&NA;. "Vecuronium bromide." Reactions Weekly &NA;, no. 1395 (March 2012): 41. http://dx.doi.org/10.2165/00128415-201213950-00142.

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29

Reich, David L., Ingrid Hollinger, Donna J. Harrington, Howard S. Seiden, Sephali Chakravorti, and D. Ryan Cook. "Comparison of Cisatracurium and Vecuronium by Infusion in Neonates and Small Infants after Congenital Heart Surgery." Anesthesiology 101, no. 5 (November 1, 2004): 1122–27. http://dx.doi.org/10.1097/00000542-200411000-00011.

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Background Neonates and infants often require extended periods of mechanical ventilation facilitated by sedation and neuromuscular blockade. Methods Twenty-three patients aged younger than 2 yr were randomly assigned to receive either cisatracurium or vecuronium infusions postoperatively in a double-blinded fashion after undergoing congenital heart surgery. The infusion was titrated to maintain one twitch of a train-of-four. The times to full spontaneous recovery of train-of-four without fade, extubation, intensive care unit discharge, and hospital discharge were documented after drug discontinuation. Sparse sampling after termination of the infusion and a one-compartment model were used for pharmacokinetic analysis. The Mann-Whitney U test and Student t test were used to compare data between groups. Results There were no significant differences between groups with respect to demographic data or duration of postoperative neuromuscular blockade infusion. The median recovery time for train-of-four for cisatracurium (30 min) was less than that for vecuronium (180 min) (P < 0.05). Three patients in the vecuronium group had prolonged train-of-four recovery: Two had long elimination half-lives for vecuronium, and one had a high concentration of 3-OH vecuronium. There were no differences in extubation times, intensive care unit stays, or hospital stays between groups. Conclusions Our results parallel data from adults demonstrating a markedly shorter recovery of neuromuscular transmission after cisatracurium compared with vecuronium. Decreased clearance of vecuronium and the accumulation of 3-OH vecuronium may contribute to prolonged spontaneous recovery times. Cisatracurium is associated with faster spontaneous recovery of neuromuscular function compared with vecuronium but not with any differences in intermediate outcome measures in neonates and infants.

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30

Wyon, Nicholas, Henning Joensen, Yuji Yamamoto, Sten G. E. Lindahl, and Lars I. Eriksson. "Carotid Body Chemoreceptor Function Is Impaired by Vecuronium during Hypoxia." Anesthesiology 89, no. 6 (December 1, 1998): 1471–79. http://dx.doi.org/10.1097/00000542-199812000-00025.

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Background Neuromuscular blocking agents reduce the human ventilatory response to hypoxia at partial neuromuscular block. It was hypothesized that vecuronium impairs carotid body chemoreceptor function during hypoxia. Method The effect of systemic administration of vecuronium on single chemoreceptor activity during hypoxia, as recorded from a single nerve fiber preparation of the carotid sinus nerve, was studied in seven mechanically ventilated New Zealand White rabbits during continuous thiopental anesthesia. During normoventilation, the isocapnic hypoxic chemosensitivity of the single carotid body chemoreceptor was measured at four levels of oxygenation; these measurements were repeated at six separate occasions: control recording before injection, after intravenous administrations of 0.1 mg and 0.5 mg of vecuronium, and then at three occasions during a 90-min recovery period. Chemoreceptor chemosensitivity during isocapnic hypoxia was expressed as a hyperbolic function: Chemoreceptor output (Hz) = a + b x PaO2(-1) (mmHg). Results Chemosensitivity was reduced after both 0.1 mg and 0.5 mg vecuronium intravenous administration compared with control measurements; the hypoxic response curve was significantly depressed after both doses (P < 0.05). Notably, there was variation in the effect of vecuronium; some chemoreceptor preparations showed only minimal impairment, whereas some showed an almost abolished response to hypoxia. The chemosensitivity remained significantly depressed at 30 and 60 min but had recovered spontaneously at 90 min after 0.5 mg vecuronium. Discussion It is concluded that vecuronium depresses carotid body chemoreceptor function to a varying extent during hypoxia and that the depression recovers spontaneously.

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31

Caldwell, James E., Tom Heier, Peter M. C. Wright, Sean Lin, Gerald McCarthy, Janos Szenohradszky, Manohar L. Sharma, Jeremy P. Hing, Marc Schroeder, and Daniel I. Sessler. "Temperature-dependent Pharmacokinetics and Pharmacodynamics of Vecuronium." Anesthesiology 92, no. 1 (January 1, 2000): 84. http://dx.doi.org/10.1097/00000542-200001000-00018.

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Background The authors evaluated the influence of temperature on the pharmacokinetics and pharmacodynamics of vecuronium because mild core hypothermia doubles its duration of action. Methods Anesthesia was induced with alfentanil and propofol and maintained with nitrous oxide and isoflurane in 12 healthy volunteers. Train-of-four stimuli were applied to the ulnar nerve, and the mechanical response of the adductor pollicis was measured. Volunteers were actively cooled or warmed until their distal esophageal temperatures were in one of four ranges: < 35.0 degrees C, 35.0-35.9 degrees C, 36.0-36.9 degrees C, and > or = 37.0 degrees C. With temperature stabilized, vecuronium was infused at 5 microg x kg(-1) x min(-1) until the first response of each train-of-four had decreased by 70%. Arterial blood (for vecuronium analysis) was sampled at intervals until the first response recovered to at least 90% of its prevecuronium level. Vecuronium, 20 microg x kg(-1) x min(-1), was then infused for 10 min, and arterial blood was sampled at intervals for up to 7 h. Population-based nonlinear mixed-effects modeling was used to examine the effect of physical characteristics and core temperature on vecuronium pharmacokinetics and pharmacodynamics. Results Decreasing core temperature over 38.0-34.0 degrees C decreases the plasma clearance of vecuronium (11.3% per degrees C), decreases the rate constant for drug equilibration between plasma and effect site (0.023 min(-1) per degrees C), and increases the slope of the concentration-response relationship (0.43 per degrees C). Conclusions Our results show that reduced clearance and rate of effect site equilibration explain the increased duration of action of vecuronium with reducing core temperature. Tissue sensitivity to vecuronium is not influenced by core temperature.

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32

Ploeger, Bart A., Jean Smeets, Ashley Strougo, Henk-Jan Drenth, Ge Ruigt, Natalie Houwing, and Meindert Danhof. "Pharmacokinetic–Pharmacodynamic Model for the Reversal of Meeting Abstracts by Sugammadex." Anesthesiology 110, no. 1 (January 1, 2009): 95–105. http://dx.doi.org/10.1097/aln.0b013e318190bc32.

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Background Sugammadex selectively binds steroidal neuromuscular blocking drugs, leading to reversal of neuromuscular blockade. The authors developed a pharmacokinetic-pharmacodynamic model for reversal of neuromuscular blockade by sugammadex, assuming that reversal results from a decrease of free drug in plasma and/or neuromuscular junction. The model was applied for predicting the interaction between sugammadex and rocuronium or vecuronium. Methods Noninstantaneous equilibrium of rocuronium-sugammadex complex formation was assumed in the pharmacokinetic-pharmacodynamic interaction model. The pharmacokinetic parameters for the complex and sugammadex alone were assumed to be identical. After development of a pharmacokinetic-pharmacodynamic model for rocuronium alone, the interaction model was optimized using rocuronium and sugammadex concentration data after administration of 0.1-8 mg/kg sugammadex 3 min after administration of 0.6 mg/kg rocuronium. Subsequently, the predicted reversal of neuromuscular blockade by sugammadex was compared with data after administration of up to 8 mg/kg sugammadex at reappearance of second twitch of the train-of-four; or 3, 5, or 15 min after administration of 0.6 mg/kg rocuronium. Finally, the model was applied to predict reversal of vecuronium-induced neuromuscular blockade. Results Using the in vitro dissociation constants for the binding of rocuronium and vecuronium to sugammadex, the pharmacokinetic-pharmacodynamic interaction model adequately predicted the increase in total rocuronium and vecuronium plasma concentrations and the time-course of reversal of neuromuscular blockade. Conclusions Model-based evaluation supports the hypothesis that reversal of rocuronium- and vecuronium-induced neuromuscular blockade by sugammadex results from a decrease in the free rocuronium and vecuronium concentration in plasma and neuromuscular junction. The model is useful for prediction of reversal of rocuronium and vecuronium-induced neuromuscular blockade with sugammadex.

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33

&NA;. "Isoflurane/vecuronium bromide." Reactions Weekly &NA;, no. 439 (February 1993): 10. http://dx.doi.org/10.2165/00128415-199304390-00048.

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&NA;. "Anaesthetics/vecuronium bromide." Reactions Weekly &NA;, no. 1105 (June 2006): 5. http://dx.doi.org/10.2165/00128415-200611050-00010.

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&NA;. "Vecuronium bromide interaction." Reactions Weekly &NA;, no. 326 (November 1990): 11. http://dx.doi.org/10.2165/00128415-199003260-00060.

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&NA;. "Vecuronium bromide overdose." Reactions Weekly &NA;, no. 334 (January 1991): 11. http://dx.doi.org/10.2165/00128415-199103340-00075.

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&NA;. "Vecuronium bromide interaction." Reactions Weekly &NA;, no. 355 (June 1991): 12. http://dx.doi.org/10.2165/00128415-199103550-00072.

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&NA;. "Vecuronium bromide interaction." Reactions Weekly &NA;, no. 529 (November 1994): 12. http://dx.doi.org/10.2165/00128415-199405290-00047.

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&NA;. "Anaesthetics/vecuronium bromide." Reactions Weekly &NA;, no. 1235 (January 2009): 7. http://dx.doi.org/10.2165/00128415-200912350-00019.

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&NA;. "Vecuronium bromide interaction." Reactions Weekly &NA;, no. 619 (September 1996): 12. http://dx.doi.org/10.2165/00128415-199606190-00035.

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41

&NA;. "Sevoflurane/vecuronium bromide." Reactions Weekly &NA;, no. 1369 (September 2011): 34. http://dx.doi.org/10.2165/00128415-201113690-00122.

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42

HEALY, T. E. J., N. D. PUGH, B. KAY, T. SIVALINGAM, and H. V. PETTS. "Atracurium and Vecuronium." Survey of Anesthesiology XXXI, no. 2 (April 1987): 91. http://dx.doi.org/10.1097/00132586-198704000-00016.

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43

Broek, L., J. M. K. H. Wierda, and P. J. Hennis. "Vecuronium and rocuronium." Anaesthesia 48, no. 4 (April 1993): 349. http://dx.doi.org/10.1111/j.1365-2044.1993.tb06973.x.

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NORMAN, J. "Resistance to vecuronium." Anaesthesia 48, no. 12 (February 22, 2007): 1068–69. http://dx.doi.org/10.1111/j.1365-2044.1993.tb07529.x.

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45

May, J. R. "Vecuronium and bradycardia." Anaesthesia 40, no. 7 (July 1985): 710. http://dx.doi.org/10.1111/j.1365-2044.1985.tb10974.x.

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DAROWSKI, M. J., W. B. A. COUTINHO, S. J. POWER, and R. M. JONES. "Vecuronium and phaeochromocytorna." Anaesthesia 41, no. 12 (December 1986): 1225–29. http://dx.doi.org/10.1111/j.1365-2044.1986.tb13008.x.

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COZANITIS, D. A. "Pain with vecuronium." Anaesthesia 41, no. 4 (April 1986): 434. http://dx.doi.org/10.1111/j.1365-2044.1986.tb13242.x.

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&NA;. "Focus on…vecuronium." Nursing 28, no. 2 (February 1998): 32cc8. http://dx.doi.org/10.1097/00152193-199802000-00018.

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&NA;. "Focus on…vecuronium." Nursing 28, no. 2 (February 1998): 32cc8. http://dx.doi.org/10.1097/00152193-199828020-00018.

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FOLDES, F. F. "BRADYCARDIA FOLLOWING VECURONIUM." British Journal of Anaesthesia 61, no. 2 (August 1988): 240–41. http://dx.doi.org/10.1093/bja/61.2.240-b.

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