Disease relevance of edrophonium

• In both the patients who were studied electromyographically, pretreatment and postplacebo responses were typical of myasthenia gravis and became normal after edrophonium [1].
• Edrophonium produced chest pain with manometric changes in 6 of 34 (18%) patients [2].
• However, LESP and PP levels after edrophonium stimulation remained significantly (P less than 0.05) reduced during hyperglycemia compared with euglycemia [3].
• When the esophagitis had resolved, the pressure response to edrophonium and pentagastrin returned to preperfusion levels [4].
• Some patients had features not usually associated with botulism including paresthesia (14%), asymmetric extremely weakness (17%), asymmetric ptosis (8%), slightly elevated cerebrospinal fluid protein values (14%), and positive responses to edrophonium chloride(26%) [5].

Psychiatry related information on edrophonium

• Growth hormone response to edrophonium in Alzheimer's disease [6].
• Metoclopramide and edrophonium caused an increase in gastroduodenal motor activity, but increased contractions were not associated with symptoms [7].

High impact information on edrophonium

• To study the ability of anticholinesterase drugs to reverse the potentially fatal paralytic effects of cobra venom, we conducted a placebo-controlled, double-blind crossover trial of intravenous edrophonium (Tensilon) in 10 adults with neurotoxic envenoming caused by bites of the Philippine cobra (Naja naja philippinensis) [1].
• Positive response to edrophonium in patients with neurotoxic envenoming by cobras (Naja naja philippinensis). A placebo-controlled study [1].
• The expiratory and inspiratory pressures, forced vital capacity, and ability to cough, speak, and swallow also improved after edrophonium [1].
• The action of AChE was independent of the subunit array of the enzyme, was not affected by edrophonium, an active site inhibitor, but it was affected by propidium, a peripheral anionic binding site ligand [8].
• SEC was observed in 5 subjects with a positive chest pain response to edrophonium and in none of the 5 subjects with a negative response [9].

Chemical compound and disease context of edrophonium

• It is concluded that blood glucose levels affect esophageal motility, acute hyperglycemia reduces LESP and impairs esophageal motility under both basal and edrophonium-stimulated conditions, and hyperglycemia reduces plasma PP levels, suggesting impaired vagal-cholinergic activity during hyperglycemia [3].
• The patient's chest discomfort and concomitant esophageal spasm were provoked by intravenous infusion of edrophonium chloride during esophageal manometry [10].
• Acid perfusion (0.1 N hydrochloric acid) and edrophonium (80 micrograms/kg intravenously) tests were placebo-controlled with a positive study defined as replication of typical chest pain [11].
• No differences between the two forms were observed for the binding of classical inhibitors such as edrophonium and propidium or inhibitors that are current or potential drugs for the treatment of Alzheimer's disease such as (-) huperzine A and E2020; tacrine inhibited the monomeric form 2-3-fold more potently than the tetrameric form [12].
• 10(-2.5) M for neostigmine, and 10(-2) M for edrophonium both in dorsal root ganglion culture and in retinal culture [13].

Biological context of edrophonium

• After edrophonium all but 1 subject showed falls in heart rate of about 6 beats/min; there were no consistent blood pressure changes [14].
• We measured the amplitudes and velocities of centrifugal saccades at the start of the task, after 3 minutes of the task (fatigue) and 1 minute after receiving IV edrophonium [15].
• Electromyogram demonstrated repetitive compound muscle action potentials in response to a single stimulus of nerve; decremental response, more prominent at higher rates of stimulation; worsening of decremental response after edrophonium injection; and normal nerve conduction velocities [16].
• In contrast, edrophonium, N-methylacridinium, and butyrylthiocholine bound to the acylation site and formed ternary complexes with the fasciculin 2-bound enzyme in which their affinities were reduced by about an order of magnitude from their affinities in the free enzyme [17].
• Cerebral evoked potential recording was used to study the oesophagus-brain axis in 10 controls and 10 patients with non-cardiac chest pain with a manometric diagnosis of either nutcracker oesophagus or diffuse spasm and a positive edrophonium test [18].

Anatomical context of edrophonium

• To improve our diagnostic yield, we studied the use of edrophonium as a provocative test for inducing esophageal chest pain in 50 symptomatic patients without coronary artery disease and in 25 age-matched controls [19].
• Carotid sinus massage following pretreatment with edrophonium in unusually high (15-20 mg, i.v.) doses broke ventricular tachycardia in all four patients [20].
• The esophagus was identified as "probably" contributing to chest pain only if the acid or edrophonium test was positive or if there was a positive correlation between symptoms and acid reflux during pH monitoring [11].
• From these results and other published data, we suggest that the pain receptor for noxious stretch and after edrophonium challenge is likely to be an 'in series' mechanoreceptor located in oesophageal longitudinal muscle [21].
• In contrast, larger doses of toxin produce an acute dysfunction of all extraocular muscle fiber types, which is responsive to edrophonium and consequently reflects partial blockade at the neuromuscular junction [22].

Associations of edrophonium with other chemical compounds

• MEASUREMENTS: 1) 24-hour three-channel esophageal manometry and two-channel pH monitoring, 2) provocation testing with intravenous edrophonium chloride and esophageal acid perfusion, and 3) Holter electrocardiography conducted during the first two tests [23].
• In a complex with edrophonium, and quaternary nitrogen of the ligand interacts with the indole of Trp-84, and its m-hydroxyl displays bifurcated hydrogen bonding to two members of the catalytic triad, Ser-200 and His-440 [24].
• Furthermore, when the acylation site ligands edrophonium or m-(N, N,N-trimethylammonio)trifluoroacetophenone form ternary complexes with AChE and thioflavin T, the fluorescence is quenched by factors of 2.7-4 [25].
• The measurements were repeated after intravenous injection of edrophonium (80 micrograms/kg) and again after 1.2 mg intravenous atropine [21].
• After administration of the choline esterase inhibitor edrophonium, the peak GH response was 14 ng/ml in healthy elderly control subjects and only 2 ng/ml in Alzheimer's patients [6].

Gene context of edrophonium

• Plasma G4 or G1 AChE did not differ in their affinity for edrophonium [26].
• Secondary to edrophonium, diethylparaquat, paraquat, morfamquat and monoquat showed lower I50 for AChE, and possessed higher inhibition selectivity (IS), expressed as the ratio of I50 for BuChE to I50 for erythrocyte AChE [27].
• For huperzine A and edrophonium, the results obtained with AChE mutants could be directly correlated with those obtained with native ChEs and site-specific mutants of human BChE [28].
• In 2 subjects sampled for 140 min. maximum serum GH levels of 19.4 and 10.2 ng/ml (from baseline values of 0.4 and 0.6 ng/ml) occurred at 65 min after edrophonium injection [29].
• Endogenous cholinergic stimulation, produced by the intravenous injection of edrophonium (10 mg), an acetylcholinesterase inhibitor, into 8 normal human subjects, resulted in an increase in the mean (+/- SE) serum growth hormone (GH) concentration from 0.6 +/- 0.1 ng/ml to 5.6 +/- 1.4 ng/ml (p < 0.01) at 40 min with no changes in serum prolactin [29].

Analytical, diagnostic and therapeutic context of edrophonium

• Fourty-four unselected patients with noncardiac chest pain were studied using conventional manometry with additional edrophonium provocation and 24-hour ambulatory esophageal pH and pressure recording with a system developed by our group [30].
• VF was induced by programmed electrical stimulation in all cases but two, in which it was induced only after edrophonium injection [31].
• Eleven of the 12 patients responding to edrophonium also responded to acid perfusion, including most of the patients with primary motility disorders [32].
• STUDY OBJECTIVE: To compare the diagnostic capabilities of traditional esophageal tests (manometry and provocative testing with acid and edrophonium) and 24-hour esophageal pH monitoring in identifying an esophageal cause of chest pain [11].
• Results indicate that acid perfusion during oesophageal manometry may be a more useful stress test than edrophonium and that the mechanism of symptom production may be similar [32].

References