Final answer:
Acetylcholinesterase inhibitors increase the level of acetylcholine at neuromuscular junctions, impacting succinylcholine's effectiveness and potentially prolonging muscle paralysis.
Step-by-step explanation:
Acetylcholinesterase inhibitors have a profound effect on succinylcholine blockade. Succinylcholine is a medication used to cause temporary paralysis by acting as a depolarizing neuromuscular blocker. It mimics acetylcholine at the neuromuscular junction but is not degraded by acetylcholinesterase, thereby causing a prolonged muscle contraction followed by paralysis. However, when acetylcholinesterase inhibitors, such as Sarin or therapeutic drugs for Alzheimer's disease and myasthenia gravis like physostigmine, neostigmine, or pyridostigmine, are present, they inhibit the degradation of acetylcholine. This accumulation of acetylcholine results in continued muscle contraction and resists the effects of succinylcholine, thus potentially prolonging its depolarizing effect and extending muscle paralysis.
Considering the therapeutic application, acetylcholinesterase inhibitors are used in the treatment of conditions such as myasthenia gravis by allowing more acetylcholine to remain at the nerve synapse, counteracting the reduced acetylcholine receptor function. However, in the context of succinylcholine blockade, especially during procedures that require muscle relaxation, the presence of an acetylcholinesterase inhibitor could lead to complications due to an extended period of muscle paralysis.