Disease relevance of suxamethonium chloride

• Malignant hyperthermia (MH) is a hypermetabolic disease triggered by volatile anesthetics and succinylcholine in genetically predisposed individuals [1].
• Succinylcholine-induced hyperkalemia complicating the neuroleptic malignant syndrome [2].
• Other potential hazards of succinylcholine administration, such as hyperkalemia and cardiac arrhythmias, are also discussed [3].
• Since the level of serum BChE activity and the duration of succinylcholine apnea are inversely correlated, this marked decrease in activity makes individuals with the J-variant more susceptible than usual subjects to prolonged apnea from succinylcholine [4].
• A 28-year-old female undergoing elective total hip replacement experienced an anaphylactic reaction to succinylcholine [5].

Psychiatry related information on suxamethonium chloride

• Succinylcholine drug interactions during electroconvulsive therapy [6].
• In three cases the superior oblique contracted vividly after administration of succinylcholine despite the presence of excyclotropia, stereopsis, torticollis (two cases) and a hypertropia that increased in adduction, in down-gaze, in adduction and down-gaze and on ipsilateral head-tilt [7].
• Patients with Huntington's chorea may respond normally to succinylcholine [8].
• Resumption of normal physical activity reverses these neuromuscular junctional changes, allowing subsequent safe succinylcholine administration [9].

High impact information on suxamethonium chloride

• In view of the widespread use of succinylcholine to induce muscle relaxation prior to ECT, it is important that the individual who administers succinylcholine in this setting be familiar with the syndrome and its treatment [10].
• A 5-week-old boy became rigid and developed cardiac arrest after receiving succinylcholine [11].
• IgE succinylcholine RAST was negative in all 23 reactor sera tested [12].
• People with genetic variants of cholinesterase respond abnormally to succinylcholine, experiencing substantial prolongation of muscle paralysis with apnea rather than the usual 2-6 min [13].
• A systematic comparison of methohexital and diazepam as anesthetics in the drug modification of ECT was done by holding atropinizaton, succinylcholine-depolarizing neuromuscular blockade, and resuscitation constant while monitoring four ECT in each of 24 patients [14].

Chemical compound and disease context of suxamethonium chloride

• Magnesium sulfate, used in the treatment of pre-eclampsia, will enhance the blocking effects of nondepolarising neuromuscular relaxants but will have no effects on the characteristics of paralysis of succinylcholine [15].
• Cholinesterases are serine hydrolases that can potentially be used as pretreatment drugs for organophosphate toxicity, as drugs to alleviate succinylcholine-induced apnea, and as detoxification agents for environmental toxins such as heroin and cocaine [16].
• Acute rhabdomyolysis following halothane anesthesia without succinylcholine [17].
• CONCLUSIONS: Although ventilatory depression preceded twitch depression, both occurred later with intramuscular mivacurium than would be expected after intravenous mivacurium or intramuscular succinylcholine [18].
• Pretreatment with nondepolarizing muscle relaxant does not decrease gastric regurgitation following succinylcholine [19].

Biological context of suxamethonium chloride

• In relation to possible succinylcholine apnoea, phenotypes AJ, AK, and JK should all be considered vulnerable [20].
• Pharmacokinetics of succinylcholine in infants, children, and adults [21].
• However, drug interactions with succinylcholine pose potential hazards to which this paper calls attention [6].
• The elimination of succinylcholine appears to follow first-order kinetics with a linear relationship between intensity of effect and logarithm of the dose [21].
• We describe a new method for measuring the in vitro rate of hydrolysis of the muscle relaxant succinylcholine [22].

Anatomical context of suxamethonium chloride

• The effect of succinylcholine on cat gastrocnemius muscle spindle afferents of different types [23].
• 1. A method of classification of muscle spindle afferents using succinylcholine (SCh) and ramp stretches has recently been described, which appears to estimate separately the strength of influence of bag1 (b1) and of bag2 (b2) intrafusal fibres [24].
• Automated determination of cholinesterase activity in plasma and erythrocytes by flow-injection analysis, and application to identify subjects sensitive to succinylcholine [25].
• Extraocular muscle fibers: ultrastructural identification of iontophoretically labeled fibers contracting in response to succinylcholine [26].
• Trigger pulses were derived from spindle afferent cell bodies of the jaw-closer muscles recorded in the mesencephalic trigeminal nucleus, and characterized by the effect of SCh on their responses to ramp-and-hold stretches [24].

Associations of suxamethonium chloride with other chemical compounds

• To study this, we applied atropine, succinylcholine and idazoxan locally to the cochlea [27].
• This automated spectrophotometric method for determination of cholinesterase activity in erythrocytes and plasma is based on measurement of the choline produced at 30 degrees C by the hydrolysis of acetyl-, butyryl-, or succinylcholine [25].
• This prospective study examined the incidence and degree of incomplete jaw relaxation in 500 children who were given intravenous succinylcholine during halothane anesthesia [28].
• METHODS: In a double-blind randomized design, the time to loss of the compound muscle action potential at the orbicularis oculi and adductor pollicis was monitored in 20 patients administered mivacurium chloride and ten patients administered succinylcholine [29].
• Serial invasive and noninvasive (systolic time interval) measurements of left ventricular performance were obtained in six healthy volunteers during general anesthesia employing the following sequence: thiopental induction, succinylcholine (prior to endotracheal intubation), and halothane--100 per cent oxygen at 1.25 and 1.75 MAC [30].

Gene context of suxamethonium chloride

• CONCLUSIONS: The current report provides direct evidence that succinylcholine-induced MMR, whole-body rigidity, and an abnormal IVCT result are associated with a mutation in the SCN4A gene [31].
• Volatile anesthetics and succinylcholine in cardiac ryanodine receptor defects [32].
• Succinylcholine and volatile anesthetics did not have a clinically significant effect on RyR2 defects [32].
• Furthermore, the diffuse extrajunctional appearance of adhalin, beta-dystroglycan, and AChR was observed after pharmacological denervation through the subcutaneous administration of succinylcholine [33].
• The effects of the H-1 receptor blocker terfenadine and the H-2 receptor blocker ranitidine have been experimentally tested in wheals induced with histamine and suxamethonium chloride [34].

Analytical, diagnostic and therapeutic context of suxamethonium chloride

• Hazards of succinylcholine administration during electrotherapy [3].
• Determination of the time-course of neuromuscular blockade following succinylcholine in infants and children allowed us to compare the rate of recovery and elimination rate constant with those determined by others in adults [21].
• The increasing longevity of the population receiving chemotherapy for physical ailments implies that greater numbers of these patients may also become candidates for ECT and therefore be at risk for adverse drug interactions with succinylcholine [6].
• It may provide a nondepolarising alternative to suxamethonium chloride for endotracheal intubation [35].
• The lack of any substantial excitation of spinothalamic neurones by intra-arterial injections of succinylcholine suggests that these group I actions may have been due to group Ib afferents from Golgi tendon organs [36].

References