Depolarizing agents

Chlorides, in particular, can present a problem because they are cathodic depolarizing agents (depolarizers) and thus negate the effectiveness of cathodic polarization techniques. 

Chloride is both a cathodic depolarizing agent (depolarizer) and a depassivating agent, and the presence of high chlorides in steam-water circuits significantly increases the risk of stress corrosion cracking of austenitic steels (type 300 stainless). 

Surprisingly few studies have been performed with purified toxins. When added externally to the water, toxins of various origins were tested on the cope-pod Tigriopus californicus. The protein phosphatase inhibitor okadaic acid (17) from red tide dinoflagellates [22] and the neuronal depolarizing agent do-moic acid (10) from diatoms [40, 41] had different effects on the herbivores (Scheme 3). Micromolar concentrations of okadaic acid (17) acted both as toxin... 

Newborn children are extremely sensitive to nondepolarizing muscle relaxants but may require three times as much depolarizing agent as an adult for an equivalent degree of block. Like newborn children, patients with myasthenia gravis are very sensitive to paralysis by d-tubocurarine but are resistant to succinylcholine. This altered responsiveness is probably due to the fewer number of functional AChRs at the end plate. Since neonates are very sensitive to d-tubocurarine, the dosage must be reduced and the degree of block closely monitored. 

Neuromuscular agents are classified as either depolarizing agents (e.g., succinylcholine) or nondepolarizing agents (e.g., tubocurarine). Succinylcholine has dual modes of action in that it possesses two phases of blocking action depolarization and desensitization. 

If muscle cells have been cut off from their neural input for a couple of weeks, they will express larger numbers of NAR molecules, even outside those membrane regions that were previously in contact with the nerve cells. If acetylcholine or another depolarizing agent is applied to these cells, they will respond with maximum contraction, and no blockade will ensue. Thus, some regulatory mechanism that suppresses muscle contraction upon sustained membrane depolarization in normal cells seems to be lost concomitantly with the denervation. 

Orndahl G, Stenberg K. Myotonic human musculature stimulation with depolarizing agents. Mechanical registration of the effects of succinyldichohne, succinyhnonochohne and decamethonium. Acta Med Scand 1962 172(Suppl 389) 3-29. 

Alkalosis is often associated with hypokalemia, in which the actions of non-depolarizing agents may be increased and those of depolarizing agents reduced. Hyperkalemia has the opposite effects, probably by lowering muscle transmembrane potential. 

The onset time for complete neuromuscular blockade is similar to that of D-tubocurarine and other non-depolarizing agents, namely 2-4 minutes. However, this is to some extent dose-dependent, and because of the relative lack of cardiovascular effects and histamine release, pancuronium can safely be given in higher dosages, thus producing good intubation conditions within 2 minutes. The dose of D-tubocurarine required to achieve similar... 

Inhalational agents potentiate muscle relaxants, which is of more clinical importance with regard to non-depolarizing agents. Tachyphylaxis and phase II block develop earlier and after smaller total doses of suxamethonium when volatile agents such as halothane, enflurane, or isoflurane (306,307) are used instead of balanced anesthesia. Halothane can increase the incidence of cardiac dys-rhjdhmias, especially bradycardia and nodal rhythm, after suxamethonium. Atropine and glycopyrrolate, particularly when given intravenously just before, afford some protection (SEDA-5,136) (308). 

Patients with thyrotoxic myopathy, as with all forms of myopathy, are exceedingly sensitive to all non-depolarizing agents. 

Contrary to their expected action, anticholinesterases potentiate the blockade produced by succinylcholine when used with non-depolarizing agents. The continued presence of succinylcholine results in repolarization of the end plate. However, despite repolarization, the end plate remains refractory to stimulation as long as succinylcholine is present. With continued exposure, the end plate begins to respond as it does to non-depolarizing agents, a non-sustained response to tetanic stimulus, which is reversed by anticholinesterases. 

Vincristine Microtubule depolarizing agent Inhibition No effect... 

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