Why lungs vasoconstrict during sympathetic stimulation?

[pizza100]

Hi. I can't understand why lungs vasoconstrict during sympathetic stimulation. Hope someone can shed some light into this matter for me.

Here's some background: My school notes say 1) Pulmonary Parasympathetic Stimulation induces Vasodilation. 2) Pulmonary Sympathetic Stimulation by Norepinephrine causes mostly vasoconstriction through alpha receptors and slight Vasodilation through beta receptors.

I tend to assume Sympathetic stimulation as fight-or-flight stimulation. If my assumption is true, then the blood vessels in the lungs should dilate during fight-or-flight (sympathetic) stimulation to increase blood flow through the lungs to supply enough oxygen to the body. Why is my thinking wrong or inconsistent with my school notes?

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[Raisenbran]

It says that it both vasoconstricts AND dilates so I THINK (and I am sure someone will correct me if I am wrong) that the poorly ventilated alveoli/lobules will vasoconstrict while the highly ventilated alveoli/lobules (which I think are the ones closer to the base of the lung?) vasodilate. This will increase the ventilation/perfusion ratio so that you are getting blood to where there is the most air and not wasting it on places where there is little air.

Again going just off memory and the way it made sense in my head but I hope it at least helps you remember that there is both vasoconstriction and dilation even if the reasoning is wrong

 

[Unzbuzzled]

It says that it both vasoconstricts AND dilates so I THINK (and I am sure someone will correct me if I am wrong) that the poorly ventilated alveoli/lobules will vasoconstrict while the highly ventilated alveoli/lobules (which I think are the ones closer to the base of the lung?) vasodilate. This will increase the ventilation/perfusion ratio so that you are getting blood to where there is the most air and not wasting it on places where there is little air.

Again going just off memory and the way it made sense in my head but I hope it at least helps you remember that there is both vasoconstriction and dilation even if the reasoning is wrong

This.

You have to make sure you differentiate between bronchiolar dilation and vascular dilation as well.

Remember, as a general rule the bronchial passages of the lungs vasodilate with sympathetic innervation. If you are running away from a tiger, you want your lungs to be open so you can get more air. This is also why albuterol is a beta2 adrenergic agonist. When you have a sympathetic rush of adrenaline, your B2 pathway is triggered and you have vasodilation of the bronchioles. Also, when you have a sympathetic response, your breathing rate goes up and so does your O2/CO2 ratio.

However, in areas of the lung that have poor ventilation, you have hypoxic pulmonary vasoconstriction of the blood vessels, which as the previous poster explained, causes an effective shunt of blood from areas of low alveolar oxygen to areas of high oxygenation.

Ultimately, low tissue oxygenation causes two things: sympathetic bronchiolar dilation, and hypoxic pulmonary vasoconstriction via the Euler– Liljestrand mechanism. So sympathetic discharge doesn't necessarily cause direct vasoconstriction, although the two are related.

 

[Smokemont]

This.

You have to make sure you differentiate between bronchiolar dilation and vascular dilation as well.

Remember, as a general rule the bronchial passages of the lungs vasodilate with sympathetic innervation. If you are running away from a tiger, you want your lungs to be open so you can get more air. This is also why albuterol is a beta2 adrenergic agonist. When you have a sympathetic rush of adrenaline, your B2 pathway is triggered and you have vasodilation of the bronchioles. Also, when you have a sympathetic response, your breathing rate goes up and so does your O2/CO2 ratio.

However, in areas of the lung that have poor ventilation, you have hypoxic pulmonary vasoconstriction of the blood vessels, which as the previous poster explained, causes an effective shunt of blood from areas of low alveolar oxygen to areas of high oxygenation.

Ultimately, low tissue oxygenation causes two things: sympathetic bronchiolar dilation, and hypoxic pulmonary vasoconstriction via the Euler– Liljestrand mechanism. So sympathetic discharge doesn't necessarily cause direct vasoconstriction, although the two are related.

While I agree with all this, isn't it a local response mediated by the partial pressure of oxygen? Whereas the original question is about sympathetic innervation, a global response?

 

[MadKanMan]

I'm just speculating here. But during a sympathetic response, heart rate is increased, so transit time through pulm vasculature is reduced, therefore compromising oxygen delivery. Maybe sympatheitc vasoconstriction happens to increase resistance and therefore slow down the blood flow through the lungs for optimal delivery of oxygen. Also, like mentioned above, NE or epi causes dilation of the airways not the pulmonary vasculature. I hope someone corrects me if I'm wrong.

 

[CrimsonKing]

As has been pointed out, the sympathetic response leads to bronchodilation and vasoconstriction.

Keep in mind, however, that this vasoconstriction is occuring at the arteriolar level, which does not play a very significant role in pulmonary circulation. While peripheral resistance will slightly increase through the pulmonary vasculature during a sympathetic response, it will not increase anywhere near enough to prevent adequate perfusion.

Also, the simultaneous bronchodilation increases the ventilation throughout the lungs which, as has also been pointed out above, can lead to VQ mismatch and an increase in dead space in the Upper Lobes (however, keep in mind that thanks to the increased pressure in the vasculature, this increase in dead space will be minimal).

 

[raiaxunmucha02]

nice job!