Muscle contraction X

tctrodotoxin batrachotoxin .local anesthetics "hemicholinium botulinus toxin procaine, Mg2+ 4-aminopyridine lack of Ca2+ excess of Ca2+

rcurare alkaloids -X"Lsnake a-toxins

—rsuccinylcholine Ldecamethonium rca'

Cholinesterase inhibitors

.veratridine

—I v ["quinine tetrodotoxin -metabolic poisons lack of Ca2+ procaine _ dantrolene

- enhancement

-X- blockade

*----depolarization and phase II block

FIGURE 9-3 Pharmacology of the neuromuscular junction. The modification of excitation-ACh secretion and nicotinic receptor activation-contraction coupling by various agents is shown on the right; an arrow marked with an X indicates inhibition or block; a plain arrow indicates enhancement or activation.

Atracurium, vecuronium, doxacurium, pipecuronium (no longer marketed in the U.S.), mivac-urium, and rocuronium are even more selective. The maintenance of cardiovascular reflex responses usually is desired during anesthesia.

Pancuronium has a vagolytic action, presumably from blockade of muscarinic receptors, that leads to tachycardia. Of the depolarizing agents, succinylcholine, at doses producing skeletal muscle relaxation, rarely causes effects attributable to ganglionic blockade. However, cardiovascular effects are sometimes observed, probably owing to the successive stimulation of vagal ganglia (manifested by bradycardia) and sympathetic ganglia (resulting in hypertension and tachycardia).

HISTAMINE RELEASE Tubocurarine produces typical histamine-like wheals when injected intracutaneously or intra-arterially in humans; some clinical responses to neuromuscular

Table 9-2

Comparison of Competitive (D-Tubocurarine) and Depolarizing (Decamethonium) Blocking Agents

Table 9-2

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