Final answer:
Prolonged use of neuromuscular blocking agents results in varying degrees of muscle paralysis, either flaccid or spastic, depending on the mechanism of action. Conditions like myasthenia gravis also involve similar symptoms but stem from an autoimmune response rather than pharmacological intervention.
Step-by-step explanation:
Prolonged use of neuromuscular blocking agents can result in various degrees of muscle paralysis. These agents function by either causing a flaccid paralysis, characterized by muscle relaxation and a sagging appearance, through inhibiting the release of acetylcholine at the neuromuscular junction; or by causing spastic paralysis, as seen in conditions like tetanus, where the toxins prevent the release of inhibitory neurotransmitters in the central nervous system.
Neuromuscular blocking agents such as d-tubocurarine work by competitively blocking the action of acetylcholine, leading to muscle relaxation and paralysis. This effect is critical during certain medical procedures, but if the agents are used too long or without proper monitoring, they can contribute to complications like prolonged muscle weakness.
It's essential to differentiate between neuromuscular blocking agents and diseases such as myasthenia gravis, which is a genetic autoimmune disorder that blocks acetylcholine receptors on muscle cells. Unlike the effects of neuromuscular blocking agents, myasthenia gravis results in progressive muscle weakness and fatigue due to an immune system malfunction rather than a pharmacological blockade.