| Indication |
For inpatients and outpatients as an adjunct to general anesthesia, to facilitate tracheal intubation, and to provide skeletal muscle relaxation during surgery or mechanical ventilation in the ICU. |
| Mechanism of action |
Cisatracurium Besylate binds to the nicotinic acetycholine (cholinergic) receptors in the motor endplate and blocks access to the receptors. In the process of binding, the receptor is actually activated - causing a process known as depolarization. Since it is not degraded in the neuromuscular junction, the depolarized membrane remains depolarized and unresponsive to any other impulse, causing muscle paralysis. |
| Absorption |
Not Available |
| Protein binding |
The binding of cisatracurium to plasma proteins has not been successfully studied due to its rapid degradation at physiologic pH. |
| Biotransformation |
The degradation of cisatracurium is largely independent of liver metabolism. Results from in vitro experiments suggest that cisatracurium undergoes Hofmann elimination (a pH and temperature-dependent chemical process) to form laudanosine and the monoquaternary acrylate metabolite. The monoquaternary acrylate undergoes hydrolysis by non-specific plasma esterases to form the monoquaternary alcohol metabolite. The monoquaternary alcohol metabolite can also undergo Hofmann elimination but at a much slower rate than cisatracurium. Laudanosine is further metabolized to desmethyl metabolites which are conjugated with glucuronic acid and excreted in the urine. |
| Route of elimination |
Biliary and urinary excretion were the major routes of excretion of radioactivity (totaling >90% of the labeled dose within 7 hours of dosing), of which atracurium represented only a minor fraction. |
| Toxicity |
Overdosage with neuromuscular blocking agents may result in neuromuscular block beyond the time needed for surgery and anesthesia. |
| Affected organisms |
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