Which two NMBs are known to produce hypotension from ganglionic blockade?

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Multiple Choice

Which two NMBs are known to produce hypotension from ganglionic blockade?

Explanation:
The selection of D-tubocurarine and Metocurine as the correct answer is rooted in their pharmacological profiles, particularly in their effects on the autonomic ganglia. Both of these neuromuscular blockers are classified as non-depolarizing agents and can cause ganglionic blockade. This means they inhibit transmission at autonomic ganglia, which can lead to a decrease in blood pressure due to the can’t exert normal sympathetic tone that counteracts vasodilation. D-tubocurarine, historically one of the first neuromuscular blockers used, has been shown to produce hypotension primarily due to its ganglionic blocking effects. Similarly, Metocurine also demonstrates this potential. As a result of these mechanisms, the use of these blockers can lead to significant cardiovascular effects, particularly hypotension. Other neuromuscular blockers listed in the choices do not possess the same propensity for ganglionic blockade. For instance, Succinylcholine is a depolarizing agent and works through a different mechanism, while Pancuronium and Vecuronium primarily work at the neuromuscular junction without significant effects on autonomic ganglia. Cisatracurium and Atracurium are also non-depolar

The selection of D-tubocurarine and Metocurine as the correct answer is rooted in their pharmacological profiles, particularly in their effects on the autonomic ganglia. Both of these neuromuscular blockers are classified as non-depolarizing agents and can cause ganglionic blockade. This means they inhibit transmission at autonomic ganglia, which can lead to a decrease in blood pressure due to the can’t exert normal sympathetic tone that counteracts vasodilation.

D-tubocurarine, historically one of the first neuromuscular blockers used, has been shown to produce hypotension primarily due to its ganglionic blocking effects. Similarly, Metocurine also demonstrates this potential. As a result of these mechanisms, the use of these blockers can lead to significant cardiovascular effects, particularly hypotension.

Other neuromuscular blockers listed in the choices do not possess the same propensity for ganglionic blockade. For instance, Succinylcholine is a depolarizing agent and works through a different mechanism, while Pancuronium and Vecuronium primarily work at the neuromuscular junction without significant effects on autonomic ganglia. Cisatracurium and Atracurium are also non-depolar

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