The fall in blood pressure caused by d–tubocurarine is due to :
**Question:** The fall in blood pressure caused by d–tubocurarine is due to:
A. Depolarization of neuromuscular junction
B. Blockade of acetylcholine receptors
C. Depolarization of myocardial cells
D. Inhibition of respiratory center in medulla oblongata
**Core Concept:**
D–tubocurarine is a muscle relaxant that belongs to the class of drugs called curare mimetics. These drugs are used to paralyze the skeletal muscles during surgery to facilitate intubation and surgery. They achieve this by inhibiting the neuromuscular junction, specifically blocking the nicotinic acetylcholine receptors on the motor endplates of the neuromuscular junction.
**Why the Correct Answer is Right:**
The fall in blood pressure caused by d–tubocurarine is due to its action on the neuromuscular junction. D–tubocurarine inhibits the release of acetylcholine from the motor neurons, leading to a decrease in the excitability of the post-junctional muscle cells. This results in a decrease in peripheral vascular resistance, which contributes to the fall in blood pressure.
**Why Each Wrong Option is Incorrect:**
A. Depolarization of neuromuscular junction: This option is incorrect because, unlike curare, d–tubocurarine does not cause direct excitation of the neuromuscular junction, but rather inhibits the neuromuscular transmission.
B. Blockade of acetylcholine receptors: Although d–tubocurarine is a curare mimetic, it does not directly block the acetylcholine receptors like other curare components do. It selectively blocks the post-junctional acetylcholine receptors, reducing the muscle cell excitability and leading to the decrease in peripheral vascular resistance.
C. Depolarization of myocardial cells: D–tubocurarine does not directly depolarize myocardial cells. Its primary action is at the neuromuscular junction, affecting the neuromuscular transmission.
D. Inhibition of respiratory center in medulla oblongata: D–tubocurarine does not primarily affect the respiratory center in the medulla oblongata. Its primary action is at the neuromuscular junction, causing a decrease in peripheral vascular resistance and leading to a decrease in blood pressure.
**Clinical Pearl:**
It is essential to distinguish between d–tubocurarine and other curare mimetics like succinylcholine or vecuronium. While these drugs also block neuromuscular transmission, the specific properties of d–tubocurarine make it advantageous in certain clinical scenarios, such as in patients with myasthenia gravis, where other cholinesterase inhibitors may exacerbate the disease. Additionally, in patients with severe respiratory distress, d–tubocurarine is preferred due to its lesser effect on the respiratory centers compared to other neuromuscular blocking agents.