Sugammadex: New Emerging Anti-dote for Muscle Relaxants

Abstract

Neuromuscular transmission at the skeletal muscle occurs when a quantum of acetylcholine from the nerve ending is released and binds to the nicotinic acetylcholine receptors on the postjunctional muscle membrane. The nicotinic acetylcholine receptors on the endplate respond by opening channels for the influx of sodium ions and subsequent endplate depolarization leads to muscle contraction. Then, acetylcholine immediately detaches from the receptor and is hydrolyzed by acetylcholinesterase enzyme. Although antiquated and long targeted for obsolescence, neostigmine and succinylcholine still serve the anesthesia community. The need to quickly establish a good intubation condition with a relaxant that will recover rapidly is fundamental to safe anesthesia practice. The major issue regarding the use of neuromuscular blocking agents has been the transition from the anesthetised, paralyzed state to the awake, fully recovered state. So is the need to restore muscle power safely and quickly at the end of surgery, by reversing a residual neuromuscular block. The use of anticholinesterases to reverse residual neuromuscular block is efficacious only if recovery is already established. Even in these circumstances, the full effect of anticholinesterases takes up to 10 min to achieve. Anticholinesterases also have muscarinic side-effects that require an anti-muscarinic to be administered concomitantly. Sugammadex is a modified γ-cyclodextrin that forms tight one-to-one complexes with rocuronium and, to a slightly lesser extent, vecuronium, reducing the free plasma concentration of these neuromuscular blocking agents (NMBAs) and rapidly terminating NMB. Sugammadex is biologically inactive, does not bind to plasma proteins, and appears to be safe. Additionally, it has