Neuromuscular blocking drugs drug interactions

Driessen JJ, Vree TB, van Egmond J, Booij LH, Crul JF. Interaction of midazolam with two non-depolarizing neuromuscular blocking drugs in the rat in vivo sciatic nerve-tibialis anterior muscle preparation. Br J Anaesth 1985 57(ll) 1089-94. 

A pharmacodynamic interaction may contribute to the reduced effect of neuromuscular blocking drugs. 

Meindewar IC, Marshall RJ. Interactions between the neuromuscular blocking drug Org NC 45 and some anaesthetic, analgesic and antimicrobial agents. Br J Anaesth 1981 53(8) 785-92. 

These are also termed as depolarizing neuromuscular blocking drugs. They are nicotinic agonists that essentially interact (just like ACH) with the post s>iiaptic nicotinic receptors to cause a depolarization of the membrane at the motor end-plate specifically. In reality, their temporary stay at the end-plate is a little longer (unlike ACH) and, therefore, the post synaptic membrane virtually remain depolarized. Because, the muscle membrane as well as the resulting contraction can only be excited by a fresh lease of depolarization, the muscle remains paralyzed ultimately. In other words, the virtual initiation for the conducted muscle impulse is due to the short-stayed fall in end-plate membrane potential, and not caused due to the ensued depolarization. 

Cammu G. Interactions of neuromuscular blocking drugs Acta Anaes iesiol Belg (2001) 52, 357-63. 

Bmga MFM, Rowan EG, Harvey AL, Bowman WC. Interactions between suxamethonium and non-depolarizii neuromuscular blocking drugs. Br J AnaesJi 99A) 72,198-204. 

Drugs that may interact with capreomycin include aminoglycosides and nondepolarizing neuromuscular blocking agents. 

In small doses, local anesthetics can depress posttetanic potentiation via a prejunctional neural effect. In large doses, local anesthetics can block neuromuscular transmission. With higher doses, local anesthetics block acetylcholine-induced muscle contractions as a result of blockade of the nicotinic receptor ion channels. Experimentally, similar effects can be demonstrated with sodium channel-blocking antiarrhythmic drugs such as quinidine. However, at the doses used for cardiac arrhythmias, this interaction is of little or no clinical significance. Higher concentrations of bupivacaine (0.75%) have been associated with cardiac arrhythmias independent of the muscle relaxant used. 

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