There are two phases to the blocking effect of<unk> . Phase 1 block Phase 1 blocking has the principal paralytic effect. Binding of<unk>  to the nicotinic acetylcholine receptor results in opening of the receptor's monovalent cation channel; a disorganized depolarization of the motor end-plate occurs and calcium is released from the sarcoplasmic reticulum. In normal skeletal muscle, acetylcholine dissociates from the receptor following depolarization and is rapidly hydrolyzed by acetylcholinesterase. The muscle cell is then ready for the next signal.<unk>  has a longer duration of effect than acetylcholine, and is not hydrolyzed by acetylcholinesterase. By maintaining the membrane potential above threshold, it does not allow the muscle cell to repolarize. When acetylcholine binds to an already depolarized receptor, it cannot cause further depolarization. Calcium is removed from the muscle cell cytoplasm independent of repolarization (depolarization signaling and muscle contraction are independent processes). As the calcium is taken up by the sarcoplasmic reticulum, the muscle relaxes. This explains muscle flaccidity rather than tetany following fasciculations. The results are membrane depolarization and transient fasciculations, followed by paralysis. Phase 2 block While this phase is not abnormal and is a part of its mechanism of action, it is undesirable during surgery, due to the inability to depolarize the cell again. Often, patients must be on a ventilator for hours if Phase 2 block occurs. It is caused by the blood concentration of<unk>  exceeding the therapeutic window. Desensitization occurs at the nerve terminal, and the myocyte becomes less sensitive to acetylcholine; the membrane repolarizes and cannot be depolarized again.
Suxamethonium chloride
Gantacurium chloride
Alcuronium chloride
Rocuronium bromide
Pancuronium bromide
Isavuconazonium
Mivacurium chloride
Rapacuronium bromide