パンクロニウムブロミド

The anticholinergic agents neostigmine, pyridostigmine, and edrophonium combined with atropine and/or glycopyrrolate can partially reverse the actions of pancuronium and serve as antidotes in the case of toxicity. Monitoring patients for adequate respiratory rate and muscle tone is crucial for determining the amount of antidote that requires administration during the reversal of pancuronium toxicity.

Drug-Induced Liver Injury Severity and Toxicity (DILIst)

pancuronium

DILI Negative

Intravenous

DOI:10.1016/j.drudis.2019.09.022

M - Musculo-skeletal system

QM - Musculo-skeletal system

Pancuronium is a non-depolarising muscle relaxant similar to curare. It acts as a competitive acetylcholine antagonist on neuromuscular junctions, displacing acetylcholine (hence competitive) from its post-synaptic nicotinic acetylcholine receptors. It is, unlike suxamethonium, a non-depolarising agent, which means, that it causes no spontaneous depolarisations upon association with the nicotinic receptor in neuromuscular junction, thus producing no muscle fasciculations upon administration. Pancuronium has no hormonal activity. It exerts slight vagolytic activity (i.e. diminishing activity of the vagus nerve) and no ganglioplegic (i.e., blocking ganglions) activity.

Nondepolarizing neuromuscular blocking agents inhibit neuromuscular transmission by competing with acetylcholine for the cholinergic receptors of the motor end plate, thereby reducing the response of the end plate to acetylcholine. This type of neuromuscular block is usually antagonized by anticholinesterase agents.

J76UF062FS

PANCURONIUM

Physiologic Effects [PE] - Neuromuscular Nondepolarizing Blockade

Established Pharmacologic Class [EPC] - Nondepolarizing Neuromuscular Blocker

Pancuronium is a Nondepolarizing Neuromuscular Blocker. The physiologic effect of pancuronium is by means of Neuromuscular Nondepolarizing Blockade.

Drugs that interrupt transmission at the skeletal neuromuscular junction without causing depolarization of the motor end plate. They prevent acetylcholine from triggering muscle contraction and are used as muscle relaxants during electroshock treatments, in convulsive states, and as anesthesia adjuvants.

Drugs that bind to nicotinic cholinergic receptors (RECEPTORS, NICOTINIC) and block the actions of acetylcholine or cholinergic agonists. Nicotinic antagonists block synaptic transmission at autonomic ganglia, the skeletal neuromuscular junction, and at central nervous system nicotinic synapses.

241 to 280 mL/kg

Plasma cl=1.1–1.9 mL/minute/kg