Succinyl choline

When Hie cholinesterase inhibitors are administered with the anticholinergic drugp, there is a potential decrease in activity of the anticholinergic drug. There is an increased risk of toxicity of theophylline when the cholinesterase inhibitors are administered with tacrine There is a synergistic effect when tacrine is administered with succinyl-choline, cholinesterase inhibitors, or cholinergic agonists (eg, bethanechol). 

Hoppe JO (1955) Observations on the potency of neuromuscular blocking agents with particular reference to succinyl-choline. Anesthesiology 16 91-124 Cullen LK, Jones RS, Snowdon DL (1980) Neuromuscular activity in the intact dog Techniques for recording evoked mechanical responses. Br Vet J 136 154-159 Keesey JC (1989) AAEE Minimonograph 33 Electrodiagnosis approach to defects of neuromuscular transmission. Muscle Nerve 12 613-626... 

Hill GE, Wong KC, Hodges MR. Potentiation of succinyl-choline neuromuscular blockade by lithium carbonate. Anesthesiology 1976 44(5) 439-42. 

The poison is powdered succinyl choline chloride which fits in a rubber and plastic pod just aft of the broadhead. When the arrow hits, the broadhead breaks the pod and dusts the wound with poison. More information from someone who knows about this would be nice to have. 

Development of reliable in-vitro predictive tests, e.g. employing serum or lymphocytes, is a matter of considerable importance, not merely to remove hazard but to avoid depriving patients of a drug that may be useful. Detection of drug-specific circulating IgE antibodies by the radioallergo-sorbent test (RAST) is best developed for penicillins and succinyl choline. 

Johnston RR, Miller RD, Way WL. The interaction of ketamine with d-tubocurarine, pancuronium, and succinyl-choline in man. Anesth Analg 1974 53(4) 496-501. 

Stirt JA, Grosshght KR, Bedford RF, Vollmer D. Defasciculation with metocurine prevents succinyl-choline-induced increases in intracranial pressure. Anesthesiology 1987 67(l) 50-3. 

Miller RD, Way WL, Hickey RF. Inhibition of succinyl-choline-induced increased intraocular pressure by nondepolarizing muscle relaxants. Anesthesiology 1968 29(l) 123-6. 

Hilgenberg JC, Stoelting RK. Characteristics of succinyl-choline-produced phase 11 neuromuscular block during enflurane, halothane, and fentanyl anesthesia. Anesth Analg 1981 60(4) 192-6. 

Ivankovich AD, Sidell N, Cairoli VJ, Dietz AA, Albrecht RF. Dual action of pancuronium on succinyl-choline block. Can Anaesth Soc J 1977 24(2) 228-42. 

Foldes FF, Hillmer NR, Molloy RE, Monte AP. Potentiation of the neuromuscular effect of succinyl-choline by hexafluorenium. Anesthesiology 1960 21 50-8. 

Management of endrin poisoning is symptomatic. Diazepam or phenobarbital is used to control convulsions. In severe cases, mechanically assisted breathing may be necessary as well as administration of succinyl-choline for muscle relaxation and control. Activated charcoal as a slurry has been reported to absorb endrin and increase its rate of excretion after oral exposure. Emesis is not recommended due to potential CNS depression or seizures. 

E22. Evans, R. T., and Wroe, J., Is serum cholinesterase activity a predictor of succinyl choline sensitivity An assessment of four methods. Clin. Chem. 24, 1762-1766 (1978). 

T4, Thesleff, S., Farmakologiska och kliniska forsok med LT I (O.O.-succinyl-cholin-jodid). (Pharmacological and clinical tests with LT 1 (O.O.-succinyl-choline-iodide).) Preliminary report. Nord, Med. 46, 1045 (1951). 

Very short duration (metabolized by plasma pseudocholinesterase see succinyl-choline below), histamine release. 

Ariens, E. J., Degroot, W. M. (1954). Affinity and intrinsic-activity in the theory of competitive inhibition. 3. Homologous decame-thonium-derivatives and succinyl-choline-esters. Archives Internationales de Pharmacodynamie et de Therapie, 99, 193-205. 

Because cholinesterase is synthesized in the liver, succinyl-choline s duration of action is elevated in the presence of liver disease. Cholinesterase inhibitors dramatically increase succinylcholine s duration of action. In patients with atypical cholinesterase, the intensity and duration of succinylcholine s effects are enhanced. 

Many compounds, including a large number of therapeutic agents, stimulate the release of histamine from mast cells directly and without prior sensitization. Responses of this sort are most likely to occur following intravenous injections of certain substances. Tubocurarine, succinyl-choline, morphine, some antibiotics, radiocontrast media, and certain carbohydrate plasma expanders may elicit the response. The phenomenon may account for unexpected anaphylactoid reactions. Vancomycin-induced red-man syndrome involving upper body and facial flushing and hypotension may be mediated through histamine release. 

Since l-n-dodecyl-3-(hydroxyiminomethyl)pyridinium iodide was indicated to be a more effective nucleophilic reagent for the hydrolysis of organophosphorus compounds, it was examined in addition to 2-PAM, 2-PAD, histidine hydrochloride, and succinyl choline as possible coatings (55,56). Among these, 3-PAD was found to be the best coating for compounds with the G agent structure, and histidine hydrochloride for compounds of the malathion type. Table 3. 

If the patient is not fuiiy relaxed (eg, if the jaw is not flaccid or neck mobility Is restricted), induce neuromuscular paralysis with succinyl-choline (1-1.5 mg/kg intravenously [IV]), rocuronium (0.6-1.2 mg/kg IV) or pancuronium (0.1 mg/kg IV), or another neuromuscular blocking agent (see p 472). Caution In children, succinylcholine may induce excessive vagal tone, resulting in bradycardia or asystole. Patients with digitalis intoxication (see p 155) may have a similar response to succinylcholine. Pretreat with atropine (0.01 mg/kg IV),... 

Nicotinic cholinergic syndrome. Stimulation of nicotinic receptors at autonomic ganglia activates both parasympathetic and sympathetic systems, with unpredictable results. Excessive stimulation frequently causes depolarization blockage. Thus, initial tachycardia may be followed by bradycardia, and muscle fasciculations may be followed by paralysis. (Examples nicotine in addition, the depolarizing neuromuscular blocker succinyl-choline, which acts on nicotinic receptors in skeletal muscle.)... 

The neuromuscular blockade due to suxamethonium (succinyl-choline) can be increased and prolonged by lidocaine, procaine and possibly procainamide. These local anaesthetics all have some neuromuscular blocking activity and may theoretically also enhance the block produced by competitive neuromuscular blockers. Increased toxicity occurred when mivacurium and prilocaine were given together for regional anaesthesia. 

Kambam JR, Dymond R, Krestow M. Effect of cimetidine on duration of action of succinyl-choline. AnesthAmlg (1987) 66, 191-2. 

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