Adverse Reactions and Interactions of the Neuromuscular Blocking Drugs

  title={Adverse Reactions and Interactions of the Neuromuscular Blocking Drugs},
  author={Doris {\O}stergaard and Jens Engbaek and J{\o}rgen Viby-Mogensen},
  journal={Medical Toxicology and Adverse Drug Experience},
SummaryThe adverse reactions seen following administration of neuromuscular blocking agents are mainly cardiovascular. Due to the lack of specificity for the nicotinic receptor at the neuromuscular junction, these agents may interact with receptors in autonomic ganglia and muscarinic receptors in the heart. Furthermore, muscle relaxants may have histaminereleasing properties. The cardiovascular effects vary with potency and specificity of the drug, depending mainly on the chemical structure… 
Drug interactions with intravenous and local anaesthetics
Relatively few clinically significant drug interactions with anaesthetics have been documented in the literature. The following should be stressed since these interactions are not readily predictable
Adverse Effects of Nondepolarising Neuromuscular Blocking Agents
SummaryNondepolarising muscle relaxants block neuromuscular transmission, acting as antagonists of the nicotinic receptors at the neuromuscular junction. Their undesired effects are frequently caused
Drug interactions with inhalational anaesthetics
The literature concerning the interactions between volatile anaesthetics, nitrous oxide and other compounds is reviewed and pentobarbitone, etomidate or a benzodiazepine should be preferred as an alternative to thiopentone when the use of adrenergic drugs peroperatively is anticipated.
Activation and Inhibition of Human Muscular and Neuronal Nicotinic Acetylcholine Receptors by Succinylcholine
The observation that succinylcholine does not inhibit the presynaptic α3β2 autoreceptor at clinically relevant concentrations provides a possible mechanistic explanation for the typical lack of tetanic fade in succinylCholine-induced neuromuscular blockade.
Blockade and Activation of the Human Neuronal Nicotinic Acetylcholine Receptors by Atracurium and Laudanosine
Adverse effects observed during atracurium administration may be attributed, at least partly, to an interaction with neuronal nicotinic receptors.
Laudanosine, an atracurium and cisatracurium metabolite.
Except for prolonged administration of atracurium in intensive care units, laudanosine accumulation and related toxicity seem unlikely to be achieved in clinical practice.
Anaphylaxis During General Anaesthesia
No specific treatment has been proven to reliably prevent the onset of anaphylactic reactions, and allergological assessment must be performed in all highrisk patients, so the only possible strategy is to avoid the drug tested positively during the allergy work-up.


Interaction of muscle relaxants and local anesthetics at the neuromuscular junction.
Findings suggest that the interaction of NM blocking agents and local anesthetics consists of true potentiation caused by the different sites of action of the two types of compounds at the NM junction.
Benzodiazepines and neuromuscular blocking drugs in patients
Neither benzodiazepine caused significant potentiation of neuromuscular blocking agents in comparison with control, however, the duration to 25% and to 75% recovery of the twitch height after vecuronium was significantly longer than with diazepam and midazolam.
The Effect of Phenytoin on the Magnitude and Duration of Neuromuscular Block Following Atracurium or Vecuronium
Although vecuronium is affected by phenytoin in an interaction similar to that previously reported with the long-acting neuromuscular relaxants, atracurium is not similarly affected.
Verapamil potentiation of neuromuscular blockade: failure of reversal with neostigmine but prompt reversal with edrophonium.
A patient on longterm therapy with verapamil is described who, 2.5 hr after the administration of 2 mg of pancuronium and 5 mg of tubocurarine, exhibited a marked degree of residual neuromuscular blockade that was resistant to reversal by neostigmine but was promptly reversed by edrophonium.
The Potentiation of Neuromuscular Blocking Agents by Quinidine
There is a definite interaction between quinidine and both the non-depolarizing and deplorarizing muscle relaxants in producing neuromuscular blockade in the cat anterior tibialis and the rat phrenic nerve-diaphragm preparations.
Potentiation of Neuromuscular Blockade by Verapamil
It is concluded that verapamil can produce potentiation of either pancuronium- or succinylcholine-induced neuromuscular block at doses within the therapeutic range.
Effects of Furosemide on the Neuromuscular Junction
High doses of furosemide inhibit non-competitively both the high- and low-affinity forms of the enzyme cyclic AMP phosphodiesterase in both soluble and particulate fractions of cat sciatic nerve.
The effect of quinidine and procainamide on the neuromuscular blocking action of suxamethonium.
  • M. Cuthbert
  • Biology, Medicine
    British journal of anaesthesia
  • 1966
Since quinidine is known to cause respiratory paralysis in man when administered intravenously during the recovery phase from suxamethonium block, it is suggested that procainamide may produce similar effects in this situation.
Presynaptic and postsynaptic actions of procainamide on neuromuscular transmission
Direct inhibitory actions on neuromuscular transmission could account for the clinical exacerbations associated with the administration of PA to patients with myasthenia gravis and other neuromUScular diseases.