hexamethonium confusion

[justpremed]

---

Members do not see this ad.

hey guys! i have a ? about hexamethonium:

from what i understand, it has the following effects:
decreased BP
increased HR
decreased CO
decreased urine output
decreased GI motility
mydriasis

does anyone understand how you get this combination of effects? it's such an odd mix of sympathetic and parasympathetic effects, and i can't figure out how/why you would get this combination of effects

thanks in advance!

 

[MudPhudHopeful]

My understanding of it is that it's a ganglionic blocker that acts at a particular subset of nicotinic receptors that are found in presynaptic autonomic ganglia of both parasympathetic and sympathetic nervous systems. Therefore, you would see a mix of sympathetic and parasympathetic side effects. The net result at a particular tissue depends on the predominant system (parasympathetic or sympathetic) innervating it.

 

[Step1Hash]

hey guys! i have a ? about hexamethonium:

from what i understand, it has the following effects:
decreased BP
increased HR
decreased CO
decreased urine output
decreased GI motility
mydriasis

does anyone understand how you get this combination of effects? it's such an odd mix of sympathetic and parasympathetic effects, and i can't figure out how/why you would get this combination of effects

thanks in advance!

it blocks the Nicotinic receptor and thus blocks all basal stimulation since the nicotinic receptor is at the preganglionic synapse of both sympathetic and parasympathetic. Since the blood vessels are sympathetic > parasympathetic at base line you get decreased BP and everything else is more parasympathetic at baseline so you get more sympathetic effects on those.

 

[justpremed]

it blocks the Nicotinic receptor and thus blocks all basal stimulation since the nicotinic receptor is at the preganglionic synapse of both sympathetic and parasympathetic. Since the blood vessels are sympathetic > parasympathetic at base line you get decreased BP and everything else is more parasympathetic at baseline so you get more sympathetic effects on those.

thanks for the quick replies!

so is it correct to say that, at the blood vessels, sympathetic blockade is greater than parasympathetic blockade? so the effect on BP is decreased BP and you have a compensatory increase in heart rate?

and, at other sites (pupil, GI motility, urine output), the parasympathetic blockade is greater, so you have mainly sympathetic effects?

and, if that's the case, what's the explanation for the cardiac output? is there a significant decrease in stroke volume?

 

[richse]

thanks for the quick replies!

so is it correct to say that, at the blood vessels, sympathetic blockade is greater than parasympathetic blockade? so the effect on BP is decreased BP and you have a compensatory increase in heart rate?

and, at other sites (pupil, GI motility, urine output), the parasympathetic blockade is greater, so you have mainly sympathetic effects?

and, if that's the case, what's the explanation for the cardiac output? is there a significant decrease in stroke volume?

Yeah, if you block the basal tone of the blood vessels then BP is going down. You can probably think of the reduced CO similar to an acid/base disturbance compensation. The HR goes up to counter the decreased BP, but it doesn't fully compensate due to decreased preload. That explanation makes sense to me although I'm not sure if it's accurate.

 

[tco]

thanks for the quick replies!

so is it correct to say that, at the blood vessels, sympathetic blockade is greater than parasympathetic blockade? so the effect on BP is decreased BP and you have a compensatory increase in heart rate?

and, at other sites (pupil, GI motility, urine output), the parasympathetic blockade is greater, so you have mainly sympathetic effects?

and, if that's the case, what's the explanation for the cardiac output? is there a significant decrease in stroke volume?

You got it.

Basically, just think that parasympathetic is the dominant tone EVERYWHERE except in the blood vessels. If you block all autonomics, the opposite will happen.

The heart - I have no idea. Are you sure that's accurate? What's your source?

 

[justpremed]

You got it.

Basically, just think that parasympathetic is the dominant tone EVERYWHERE except in the blood vessels. If you block all autonomics, the opposite will happen.

The heart - I have no idea. Are you sure that's accurate? What's your source?

this is from dr. brian jenkins in one of the DIT lectures.

 

[ChessMaster3000]

Hey, saw this old thread and had another question I was hoping someone could answer. If you are giving a sympathomimetic OR sympatholytic in conjunction with hexamethonium, does it really matter what hexamethonium does, since the sympathomimetic/lytic would be acting at the end-0rgan, while hexamethonium acts at the ganglion?

 

[Myxedema]

There could be a question like that. For example, let's say a researcher is testing drug X. When drug X is given alone to a rat, the researcher notes contraction of the radial muscle of the eye. When the researcher administers drug X concomitantly with hexamethonium, this response becomes decreased. However, when norepinephrine is added, the researcher notes further contraction of the radial muscle. What could be the drug X? a) Neostigmine, b) Tetrodotoxin, c) Fentanyl , d) Vesamicol, e) Cocaine

 

[ChessMaster3000]

There could be a question like that. For example, let's say a researcher is testing drug X. When drug X is given alone to a rat, the researcher notes contraction of the radial muscle of the eye. When the researcher administers drug X concomitantly with hexamethonium, this response becomes decreased. However, when norepinephrine is added, the researcher notes further contraction of the radial muscle. What could be the drug X? a) Neostigmine, b) Tetrodotoxin, c) Fentanyl , d) Vesamicol, e) Cocaine

Myx I'll go with A.

 

[ChessMaster3000]

Myx I'll go with A.

Also, while we are at it, can you think of a test question which tetrodotoxin is used? I know it's a Na channel blocker but I am struggling to figure out how to incorporate that into my knowledge

 

[Myxedema]

Also, while we are at it, can you think of a test question which tetrodotoxin is used? I know it's a Na channel blocker but I am struggling to figure out how to incorporate that into my knowledge

A 21-year-old man is brought to the emergency department unable to breath. His vitals are: T - 37.6 C; BP - 90/60 mm Hg, P - 55/min, RR - 6/min. He was given O2 via mask in the field, and his SaO2 in the emergency department measures 89%. His fiancée states that they were dining in a Japanese restaurant when the patient suddenly started to complain about a tingling sensation in his arms. In a few moments later, his face started to turn blue and he started gasping for air, as she was calling 911. When questioned, she says that he ordered a Fugu puffer fish, while she had some onigiri (rice balls). There was no other customer having a similar episode. What is the mechanism of action of the most likely cause of this patient's symptoms? a) Depletes neurotransmitter storage, b) Blocks ACh release from nerve terminal, c) Blocks NE release from nerve terminal, d) Blocks voltage-gated Na+ channels, e) Inhibits AChE enzyme

 

[ChessMaster3000]

A 21-year-old man is brought to the emergency department unable to breath. His vitals are: T - 37.6 C; BP - 90/60 mm Hg, P - 55/min, RR - 6/min. He was given O2 via mask in the field, and his SaO2 in the emergency department measures 89%. His fiancée states that they were dining in a Japanese restaurant when the patient suddenly started to complain about a tingling sensation in his arms. In a few moments later, his face started to turn blue and he started gasping for air, as she was calling 911. When questioned, she says that he ordered a Fugu puffer fish, while she had some onigiri (rice balls). There was no other customer having a similar episode. What is the mechanism of action of the most likely cause of this patient's symptoms? a) Depletes neurotransmitter storage, b) Blocks ACh release from nerve terminal, c) Blocks NE release from nerve terminal, d) Blocks voltage-gated Na+ channels, e) Inhibits AChE enzyme

Does it block only PNS sodium channels?

 

[menniscus]

i found this old thread but i really have a question...
how is it possible that neostigmine causes constriction of radial muscle? that would cause mydriasis right?
i thought neostigmine would cause miosis...
thanks!