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7.4:

Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacological Actions

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Pharmacology
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JoVE 핵심 Pharmacology
Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacological Actions

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Nondepolarizing neuromuscular blockers inhibit muscle contraction by preventing the depolarization of muscle cell membranes. When administered at low doses, they compete with acetylcholine, a neurotransmitter, to bind to its receptor site. So they are also known as competitive blockers. They are usually given with anesthetics during surgeries to produce complete muscle relaxation. Their collective action allows a lower dosage of anesthetics to achieve the desired effect, decreasing the risks associated with general anesthesia. When a competitive blocker is injected, small, rapidly moving facial and hand muscles are paralyzed first, followed by the limb, neck and trunk muscles. Next, larger muscles, like the intercostal muscles, are affected. The last muscle to paralyze is the diaphragm. When the drug administration is stopped, these muscles recover rapidly in the reverse order, with the diaphragm recovering first and facial muscles last. Most competitive blockers cannot penetrate the blood-brain barrier but can affect the autonomic ganglia. Such drugs, like atracurium, release histamine into the systemic circulation, causing a drop in blood pressure, flushing, and bronchospasm.

7.4:

Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacological Actions

Nondepolarizing neuromuscular blockers prevent the membrane depolarization of muscle cells and inhibit muscle contraction. These are usually administered with anesthetics to achieve complete muscle relaxation. Upon administration, these drugs first block the small, rapidly contracting muscles of the face and hands, followed by the larger muscles of the trunk and the intercostal muscles. The diaphragm is the last muscle to be affected.

Although all competitive neuromuscular blockers are designed to produce desirable pharmacological actions, they can also have adverse effects mediated by histamine or autonomic receptors. Drugs like tubocurarine and atracurium lead to histamine release into the systemic circulation. Histamine can cause a fall in blood pressure or hypotension. Pancuronium increases the heart rate and cardiac output. The release of larger doses of histamine can block autonomic ganglions, which affects cardiovascular functions,  increasing the heart rate and blood pressure. Bradycardia occurs initially, followed by tachycardia. Prolonged administration of drugs like succinylcholine can result in cardiac arrhythmias and even cardiac arrest in some patients. Other patients may experience flushing, bronchospasm, and increased respiratory secretions.