ENLON PLUS- edrophonium chloride and atropine sulfate injection, solution
Mylan Institutional LLC
Rx only
ENLON-PLUS (edrophonium chloride, USP and atropine sulfate, USP) Injection, for intravenous use, is a sterile, nonpyrogenic, nondepolarizing neuromuscular relaxant antagonist. ENLON-PLUS is a combination drug containing a rapid acting acetylcholinesterase inhibitor, edrophonium chloride, and an anticholinergic, atropine sulfate. Chemically, edrophonium chloride is ethyl (m-hydroxyphenyl) dimethylammonium chloride; its structural formula is:
Chemical Structure
Molecular Formula: C10 H16 ClNO
Molecular Weight: 201.70
Chemically, atropine sulfate is: endo-(�)-alpha-(hydroxymethyl)-8-methyl-8-azabicyclo [3.2.1]oct-3-yl benzeneacetate sulfate (2:1) monohydrate. Its structural formula is:
Chemical Structure
(click image for full-size original)
Molecular Formula: (C17 H23 NO3 )2 �H2 SO4 �H2 O
Molecular Weight: 694.84
ENLON-PLUS contains in each mL of sterile solution:
5 mL Ampule: 10 mg edrophonium chloride and 0.14 mg atropine sulfate compounded with 2.0 mg sodium sulfite as a preservative and buffered with sodium citrate and citric acid. The pH range is 4.0-5.0.
CLINICAL PHARMACOLOGY
Pharmacodynamics
ENLON-PLUS (edrophonium chloride, USP and atropine sulfate, USP) Injection is a combination of an anticholinesterase agent, which antagonizes the action of nondepolarizing neuromuscular blocking drugs, and a parasympatholytic (anticholinergic) drug, which prevents the muscarinic effects caused by inhibition of acetylcholine breakdown by the anticholinesterase. Edrophonium chloride antagonizes the effect of nondepolarizing neuromuscular blocking agents primarily by inhibiting or inactivating acetylcholinesterase. By inactivating the acetylcholinesterase enzyme, acetylcholine is not hydrolyzed as rapidly by acetylcholinesterase and is thereby allowed to accumulate. The greater quantity of acetylcholine reaching the sites of nicotinic cholinergic postjunctional receptors improves transmission of impulses across the myoneural junction. The concomitant, unavoidable accumulation of acetylcholine at the sites of muscarinic cholinergic transmission occurring at the parasympathetic, postganglionic receptors of the autonomic nervous system, may cause bradycardia, bronchoconstriction, increased secretions, and other parasympathomimetic side effects. The magnitude of these muscarinic side effects can be expected to vary from patient to patient depending upon the amount of vagal nerve activity present. Atropine sulfate counteracts these side effects.
Intravenous edrophonium chloride in doses of 0.5 to 1.0 mg/kg promptly antagonizes the effects of nondepolarizing muscle relaxants reaching the maximum antagonism within 1.2 minutes. A plateau of maximal antagonism is sustained for 70 minutes1. Intravenous atropine sulfate has an immediate effect on heart rate which reaches a peak in 2 to 16 minutes and lasts 170 minutes after an average 0.02 mg/kg dose.
