Disease relevance of Atracurium

• Determination of continuous atracurium infusion rate in dogs undergoing whole-body hyperthermia [1].
• Many practitioners have thus chosen to use atracurium instead of longer-acting neuromuscular blockers when muscle relaxation is required in the supportive management of critically ill patients [2].
• In conclusion, corticosteroid-treated patients with severe asthma who undergo prolonged neuromuscular paralysis are at significant risk for the development of muscle weakness, and the risk of weakness is not reduced by use of atracurium [3].
• Influence of extreme obesity on the body disposition and neuromuscular blocking effect of atracurium [4].
• We here report a case of prolonged paresis after the administration of atracurium [2].

Psychiatry related information on Atracurium

• Anaesthesia, atracurium and Huntington's chorea [5].
• Succinylcholine 2-5 mg or atracurium 10-15 mg were given on five separate occasions to a 24-year-old, 64 kg woman homozygous for atypical plasma cholinesterase who was undergoing electroconvulsive therapy (ECT) [6].

High impact information on Atracurium

• Atracurium infusion rates appear to be linear and related to body temperature from 26-42 degrees C. Clinically useful neuromuscular blockade in dogs may be obtained during whole-body hyperthermia by utilizing the 42 degrees C atracurium infusion rate throughout the 38-42 degrees C heating phase [1].
• Paralyzed patients received either TOF monitoring with a goal of three twitches or best clinical assessment while receiving atracurium by continuous infusion [7].
• The goal of this study was to develop a murine model of atracurium-induced bronchoconstriction in which to evaluate the mechanism of action of this airway response [8].
• Genetic susceptibility to atracurium-induced bronchoconstriction [8].
• Pharmacokinetics and pharmacodynamics of atracurium obtained with arterial and venous blood samples [9].

Chemical compound and disease context of Atracurium

• CONCLUSIONS: Cisatracurium, an isomer of atracurium, appears to be a suitable agent for providing muscle relaxation in critically ill patients [10].
• To determine the influence of renal function on the pharmacology of atracurium, 10 patients with normal renal function and 10 with renal failure (scheduled for cadaver kidney transplant) were anesthetized with nitrous oxide and halothane [11].
• The present study was designed to investigate whether D,L-laudanosine (a breakdown product of the neuromuscular relaxant atracurium besylate) interacts with benzodiazepinergic receptors or muscarinic receptors, both of which are involved in epilepsy and other types of seizures [12].
• Comparison of the neuromuscular recovery after paralysis with atracurium versus vecuronium in an ICU patient with renal insufficiency [13].
• OBJECTIVE: To compare haemodynamic and gas exchange effects after either atracurium or pancuronium given to ventilated neonates with respiratory failure [14].

Biological context of Atracurium

• It is concluded that forearm venous levels do not correspond to adductor pollicis neuromuscular blockade and the kinetics and kinetic-dynamic relationship for atracurium are heavily dependent on sampling site [9].
• Atracurium is a competitive neuromuscular blocking drug which undergoes Hofmann degradation and ester hydrolysis in plasma [15].
• RESULTS: Maximal blood pressure and heart rate changes in all groups of patients receiving 51W89 were small and similar to those observed in patients receiving 2 times the ED95 of atracurium [16].
• Clinical pharmacology of vecuronium and atracurium [17].
• The protein binding of atracurium was identical for both sham and injured groups [18].

Anatomical context of Atracurium

• To determine the influence of sampling site on atracurium pharmacokinetic-pharmacodynamic relationships, blood was drawn simultaneously from the radial artery and peripheral vein during a 20-minute period after injection of atracurium, 0.2 mg/kg, in eight patients [9].
• While monitoring the thenar EMG response to ulnar nerve stimulation, the authors gave either 105, 150, 210, or 300 micrograms/kg of atracurium to 60 patients [19].
• At 10, 20, 30, 40, 60, and 90 days after injury, rats were anesthetized and ventilated and the strength of contraction of their gastrocnemius produced by supramaximal stimulation of the sciatic nerve was measured before and after a bolus of atracurium (2.0 mg/kg) was administered [18].
• Adding atracurium to a propofol-fentanyl induction regimen significantly improved the quality of tracheal intubation and decreased postoperative hoarseness and vocal cord sequelae [20].
• The authors conclude that atracurium in doses which produce adequate skeletal muscle relaxation during steady-state enflurane anesthesia produces no clinically significant alteration in hemodynamic variables [21].

Associations of Atracurium with other chemical compounds

• Increasing UV/MV with longer drug injection to delivery intervals have been demonstrated for drugs with a high molecular weight, such as atracurium, but not for those with a low molecular weight, such as vecuronium, while conflicting results have been reported for pancuronium [22].
• The pharmacokinetics of atracurium, laudanosine and the quaternary alcohol were studied in patients with normal and impaired renal function following intravenous administration of atracurium [23].
• Cisatracurium besilate, one of the 10 stereoisomers that comprise atracurium besilate, is a nondepolarising neuromuscular blocking agent with an intermediate duration of action [24].
• 2. Following nasotracheal intubation and ventilation (oxygen saturation, O2,Sat, 98-100% and end-tidal CO2, PET,CO2, 30-40 mmHg), total neuromuscular blockade was induced by a rapid injection of atracurium (> 2.5 mg kg-1) and complete paralysis was maintained with an infusion (5 mg (kg h)-1) [25].
• When anesthetic conditions and mechanical ventilation were stable, patients were randomly given 0.5 mg/kg atracurium or 0.1 mg/kg vecuronium over 5-10 s, and a blinded observer recorded cardiovascular, pulmonary, and cutaneous signs of adverse reactions for 6 min [26].

Gene context of Atracurium

• In conclusion, TIVA with propofol, sufentanil and atracurium does not seem to have a significant effect on IL-1beta, IL-4, IL-6, TNF-alpha and IFN-gamma release [27].
• Combined H1 and H2 receptor blockade attenuates the cardiovascular effects of high-dose atracurium for rapid sequence endotracheal intubation [28].
• As part of departmental quality assurance, we examined the degree of postoperative residual curarization (PORC) following atracurium [29].
• After atracurium, time50-75% was shortened by the tetanic stimulation from a control of 6.3 +/- 1.1 to 5.0 +/- 1.3 min (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)[30]
• In an effort to identify the mechanism(s) responsible for the resistance to nondepolarizing muscle relaxants, the density of acetylcholine receptors (AChR) and the activity of acetylcholinesterase (AChE) were determined in rats following a 30% total body surface thermal injury at a time when resistance to atracurium is maximum [31].

Analytical, diagnostic and therapeutic context of Atracurium

• To quantify the changes in plasma concentrations of atracurium and laudanosine induced by the lack of hepatic function and circulation, the authors studied nine domestic pigs (22-25 kg) undergoing an orthotopic liver transplantation, and three control animals without surgery, using atracurium as the muscle relaxant [32].
• Total and unbound plasma concentrations of atracurium for 50% paralysis were measured using high-performance liquid chromatography [33].
• OBJECTIVE: Atracurium is sometimes used for muscle relaxation in patients undergoing mechanical ventilation [34].
• RESULTS: Application of atracurium in the perfusion medium resulted in a dose-dependent enhancement of excitatory synaptic responses averaging 48.7 +/- 4.3% at a concentration of 10 nM [35].
• In the control group, plasma concentrations of atracurium remained stable between 6.5-8.0 micrograms/ml following initial bolus injection; plasma concentrations of laudanosine increased during the first 60 min, then remained stable between 0.69-0.74 micrograms/ml up to the end of the study [32].

References