Language
Country/Area
No result found
Exploring the neuromuscular junction: How do these drugs paralyze our muscles?
Neuromuscular blocking drugs (NMBAs) paralyze the affected skeletal muscles by blocking transmission at the neuromuscular junction. These drugs act primarily through their action on postsynaptic acetylcholine (ACh) receptors. In clinical applications, neuromuscular blocking drugs assist anesthesia. The first purpose is to paralyze the vocal cords and make tracheal intubation smoother. The second purpose is to optimize the field of view of surgical operations and promote muscle activation by suppressing spontaneous ventilation. Relax.
These drugs help reduce patient movement, respiratory or ventilatory dyssynchrony and reduce the ventilatory pressures required during laparoscopic surgery.
However, the use of appropriate doses of neuromuscular blocking drugs may also paralyze the muscles that control breathing (such as the diaphragm), so a mechanical ventilator is necessary to maintain proper breathing during this type of anesthesia. This type of drug has a variety of indications in intensive care units and can help reduce hoarseness and reduce damage to vocal cords during tracheal intubation. In addition, neuromuscular blocking drugs play a key role in promoting mechanical ventilation in patients with poor lung function.
The patient is still aware of pain even after total further conduction block has occurred, which means that general anesthetics and/or analgesics need to be administered to prevent anesthetic awareness.
Nomenclature
Neuromuscular blocking drugs are generally divided into two main categories: Pachycurares, which are large molecules with non-depolarizing activity; and Leptocurares, which are thin molecules with depolarizing activity. These drugs are also often classified based on their chemical structure.
Non-depolarizing blockers
The principal feature of non-depolarizing neuromuscular blocking drugs is that they act by competitively preventing the binding of acetylcholine to its receptors. Representatives of this class of drugs include tubular and steroid-structured drugs, such as Tubocurarine and Pancuronium. These drugs require blocking approximately 70% to 80% of ACh receptors for effective neuromuscular conduction failure to occur. How quickly a drug works depends on its potency, and the more potent it is, the slower it tends to start working.
Depolarization blockers
Drugs such as succinylcholine, for example, work by depolarizing the membranes of skeletal muscle fibers. These drugs are more resistant to cholinesterase than other drugs, leaving muscle fibers in a state of continuous depolarization and no longer responding to ACh stimulation. Trianylcholine causes muscle paralysis briefly and rapidly, usually within seconds.
The rapid-acting properties of this class of drugs make them important in emergency intubation and rapid sequence intubation.
Drug comparison
The main difference in this class of drugs is how they restore neuromuscular conduction. Non-depolarizing muscle relaxants can be reversed by cholinesterase inhibitors, whereas depolarizing agents are sustained under the influence of cholinesterase inhibitors, which results in a prolongation of their effects. After clinical use of such drugs, patients may experience muscle tremors and, after a period of time, complete paralysis.
Through the influence of neuromuscular junction squeeze potential, these drugs jointly regulate muscle contraction and relaxation. Operations at the neuromuscular junction involve complex physiological mechanisms, and the pharmacology and structural properties of drugs are also closely related. These neuromuscular blocking drugs not only play a role during surgery, but also play a vital role in life support for critically ill patients.
As science advances and these drugs are further studied, will new neuromuscular blockers be discovered that are faster and more effective in the future?
