Depolarizing neuromuscular blocking drugs

Mechanism of action of depolarizing neuromuscular blocking drugs. 

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. 

The effects of non-depolarizing neuromuscular blocking drugs can be potentiated and their actions prolonged by large doses of local anesthetics, because of depression of nerve conduction, inhibition of acetylcholine formation, mobilization, and release, reduced postsynaptic receptor channel opening times, and reduced muscle contraction (370). 

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. 

Bowman WC (1980) A new non-depolarizing neuromuscular blocking drug. Trends Pharmacol Scil 263-266... 

Zaimis E, Head S (1976) Depolarizing neuromuscular blocking drugs. In Handbook of experimental pharmacology 42 the neuromuscular junction. Springer, Berlin (Chap. 4a)... 

The second group of neuromuscular blocking drugs are those of the depolarizing type. These compounds resemble the structure of two molecules of... 

All of the available neuromuscular blocking drugs bear a structural resemblance to acetylcholine. In fact, succinylcholine is two acetylcholine molecules linked end-to-end (Figure 27-2). In contrast to the single linear structure of succinylcholine and other depolarizing drugs, the nondepolarizing... 

From animal experiments (8) it seems hkely that drug interactions with atracurium will be similar to those for other non-depolarizing neuromuscular blocking agents. Laudanosine has been reported to increase the MAC for halothane in animals (61). 

Quinidine is a non-depolarizing muscle blocker and potentiates the effects of neuromuscular blocking drugs (80). 

There are two types of neuromuscular blocking drugs used during surgery nondepolarizing neuromuscular blockers and depolarizing neuromuscular blockers. 

Pyrantel, as pyrvinium, is available as the extremely insoluble and nonabsorbed pamoic acid salt one oral dose cures pinworm and Ascaris infections. It is curious that whipworm and threadworm infections do not respond. The drug acts as a depolarizing neuromuscular blocking agent (Chapter 8) on worms, which are then paralyzed. In Ascaris muscle strips it is 100 times more active than acetylcholine. 

These are also known as the competitive neuromuscular blocking drugs. In a situation, when the impulses in the somatic nerve arrive at the specific region located in the nerve terminals in the motor end-plate, they eventually elicit the release of acetylcholine (ACh), which in turn gets diffused to the post-synaptic motor end-plate membrane. Thus, ACH combines with nicotinic cholinergic receptors to activate them that ultimately leads to the opening of transmembrane ion channels, ion-flow, and as a result affords membrane depolarization. Importantly, end-plate membrane depolarization is usually accompanied by depolarization of the muscle membrane and ultimately leads to muscle contraction In short, any plausible and feasible interruption of the aforesaid squence of events gives rise to the muscular paralysis. 

The nicotinic receptors on the neuromuscular end plate apparatus are similar but not identical to the receptors in the autonomic ganglia (Table 7-1). Both types respond to acetylcholine and nicotine. (However, as noted in Chapter 8, the receptors differ in their structural requirements for nicotinic blocking drugs.) When a nicotinic agonist is applied directly (by iontophoresis or by intra-arterial injection), an immediate depolarization of the end plate results, caused by an... 

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