Vagus Nerve?

[FL_Medic]

Ok, I am only asking this question because I have never completely understood how Atropine works at the cellular level. Maybe I should just forget it and move on, but I like to know this stuff so here it goes.

From my understanding Atropine works on the Vagus nerve which is located in the R atrium, which explains why we do not administer it in a high grade AV block. Exactly how does this interaction occur? Normally neurotransmitters travel from one neuron to another across a synapse or cleft. What part of the vagus nerve is located in the atrium? The dendrite? And if so how does it receive the medication? From the blood?

Maybe a stupid question, let me know if anyone has the answer.

[AZCEP]

The vagus nerve (Cranial nerve X) directly innervates the right atria, near the SA node, and the AV junction. The connection that you speak of would be the dendrite. The nerve itself transmits it's message with acetylcholine (ACh) to the given tissue that it comes into contact with.

The trouble with using atropine for the high grade AV block is due to the loss of conduction through the AV node more than ACh's effect on the atria. When the vagus nerve is stimulated, conduction through the AV node slows down. This accounts for the effectiveness of most vagal maneuvers on reentry tachycardias. Atropine works through a counteraction of the ACh. It basically blocks the release of the neurotransmitter from the dendrite into the synapse. Less ACh released, less cholinergic effect (S-L-U-D-G-E) from the muscarinic receptors that atropine works on.

ACh is contained fairly well within the synapses. Should a cholinergic agent make it into the blood stream, the effects will be much longer acting. Check the organophosphates, for example. Neurotransmitters don't have a half-life that allows them to be directly dangerous to the functional level of the cells. Problems arise when the neurotransmitters stimulate the release of other hormones that will last longer.

The short answer, Atropine counteracts cholinergic effects on the muscarinic receptor site.

[FL_Medic]

Thanks.

[Ridryder 911]

+10 to AZCEP! Now this is what the forums all about !...

R/r 911

[FL_Medic]

+10 to AZCEP! Now this is what the forums all about !...

R/r 911

hey what about the question?

[dzmohr]

WOW!!! I was just going to say what happens in Vegus stays in Vegus but his answer was better!

I have NO idea why I had to say that but it had to be said, I was sincere about it being a very good explanation though!

[emsbrian]

Bows to AZCEP, way to slap that one down, good job.

[AZCEP]

hey what about the question?

The question of how does the atropine have an effect, has been answered. It works to counteract the ACh at the muscarinic receptor site.

The connection of the vagus nerve in the atrial/junctional tissue is the dendrite. The synapse is the space between the dendrite and the effector organ/tissue. In this case the SA/AV nodal tissue.

Atropine does not work directly on the vagus nerve. Insert "what happens in vagus, stays in vagus" here. The atropine is working on the muscarinic receptor site, where the ACh is taking effect. Similar to how Narcan competes with opioids at specific narcotic receptors. The blood is providing a mechanism for the drug to be circulated to the receptor sites. It will not have a direct effect on the vagus nerve.

For illustration purposes only:

Some patients with seizure disorders have a device implanted that will stimulate the vagus nerve prior to a seizure. This action increases the activity of the parasympathetic nervous system, slowing the generation of impulses in the CNS.

These patients will still respond to atropine, because the drug is going to blunt some of the actions of the PNS.

The patient that has had a heart transplant, on the other hand, won't respond well, if at all, to atropine because the vagus nerve no longer has direct effects on the heart. Atropine can work on the other organ systems that the vagus nerve innervates above the level of the transection.

Is that a better answer?

[fiznat]

I'm sure a lot of you guys know this already, but just to add to the discussion:

Acetylcholine is mediated by another enzyme called Acetylcholinesterase, which serves the function of breaking down Acetylcholine. Like AZECP said, neurotransmitters like this do not metabolize as easially like many other chemicals do in the body, so this second enzyme is necessary to break it down when levels get too high.

Organophosphates are potent neurotoxins because they work against Acetylcholinesterase. ...Meaning they destroy the enzyme that breaks down Acetylcholine, resulting in an excess of that neurotransmitter, and an increase of vagal stimulation. ...Hence the SLUDGE signs + symptoms, which are in effect the results of an overactive parasympathetic nervous system.

We combat Organophosphate overdose with Atropine because, like Acetylcholinesterase, Atropine works to break down Acetylcholine and decrease parasympathetic tone.

Learing about drugs on the cellular level is fun!

[ERDoc]

Just to clean up things a bit. Acetylcholine (Ach) is released by the presynaptic neuron into the synaptic cleft. Once in the cleft the Ach binds with Ach receptors on the post-synaptic target (the SA node in this case). Acetylcholinesterase is the enzyme that breaks down Ach once it is released from the presynaptic neuron. This limits the action of the Ach. Atropine competes with the Ach to bind with the postsynaptic receptors. The difference is that atropine does not cause any postsynaptic events. It does not actually do anything to the Ach. In organophosphate(OP) poisoning, the OP binds with the Acetylcholinesterase, preventing it from breaking down Ach. This allows the Ach to exert its affects without being inhibited. Atropine is used so that the Ach cannot bind to the postsynaptic receptor in OP poisoning.