CISATRACURIUM

​

Cisatracurium is a non-depolarizing neuromuscular blocking agent (NMBA) that is commonly used in anesthesia practice. It works by binding to and inhibiting the nicotinic acetylcholine receptors at the neuromuscular junction, leading to muscle relaxation and paralysis. Cisatracurium is important in anesthesia for several reasons:

​

​

​1. Facilitation of endotracheal intubation: During general anesthesia, endotracheal intubation is often performed to secure the patient's airway and provide mechanical ventilation. Cisatracurium, as a neuromuscular blocking agent, helps facilitate intubation by providing adequate muscle relaxation and reducing the risk of airway injury.

2. ​Improved mechanical ventilation: In some cases, patients under general anesthesia may require mechanical ventilation. Cisatracurium can help optimize ventilation by reducing spontaneous respiratory movements and ensuring adequate synchronization with the ventilator.

3. Devoid of histamine release: Cisatracurium, in contrast to atracurium, is devoid of histamine-releasing effects, so cardiovascular changes do not accompany the rapid intravenous administration of even large doses of cisatracurium.

​

Here are the main steps in cisatracurium's mechanism of action:

​

1. Binding to nicotinic acetylcholine receptors: Cisatracurium competes with the neurotransmitter acetylcholine (ACh) for binding to the alpha subunits of nicotinic acetylcholine receptors at the neuromuscular junction. These receptors are ligand-gated ion channels found on the motor endplate of skeletal muscle fibers.

2. Inhibition of ion channel opening: When cisatracurium binds to the nAChRs, it prevents the receptor from undergoing a conformational change and opening the ion channel, thus inhibiting the influx of sodium ions and the depolarization of the muscle cell membrane.

3. Prevention of muscle contraction: The inhibition of muscle cell depolarization prevents the initiation of muscle contraction by blocking the release of intracellular calcium from the sarcoplasmic reticulum, which is required for muscle contraction.

4. Muscle paralysis: The antagonism of nAChRs by cisatracurium leads to muscle paralysis, which starts with small, rapidly contracting muscles (such as the muscles controlling eye movement) and progresses to larger muscles, including those involved in respiration.

5. After the drug is metabolized and its concentration decreases, acetylcholine molecules can once again bind to the nAChRs and activate them, leading to the restoration of neuromuscular transmission and muscle function.

​​

                                                                                         Key points about Cisatracurium

​

• Cisatracurium is a stereoisomer of Atracurium that is four times more potent.

 

• Undergoes degradation in plasma at physiological pH and temperature by organ-independent.

 

• Metabolism and elimination are independent of renal or liver failure.

 

• Cisatracurium shares with Atracurium the production of laudanosine.

 

• The amount of laudanosine produced for the same extent and duration of neuromuscular blockade is much less than Atracurium.

 

• It does not alter heart rate or blood pressure, nor does it produce autonomic effects.

 

​​

 

​​

​

​

​

​

​

​

​

​

​

​

​

​

​

​

​

​

​

 

​​

​​