Hering-Breur Reflex

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Alde8127

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Just out of interest, if the vagus is damaged in children, then obviously the pulmonary stretch receptors lose innervation and they can't promote expiration in over-stretch, but does that mean that elastic tissue is also damaged as the lung only deflates at a normal rate, or can the Botzinger complex cause the expiration?

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I have no idea what the Botzinger complex is (you'd better explain), and I read about the Hering breuer reflex ages ago. But as far as I remember, its purpose is to limit excessive stretching of the lungs. It doesn't cause expiration. Resting expiration is a passive process, the muscles that expanded and diminished the IPP relax, and the lung shrinks under the force of its recoil. So I don't think expiration should suffer in such a case.

If you want to increase your rate of expiration, you'd be using your accessory muscles (internal and innermost intercostals, abdominal muscles), so I don't think the vagus has a role here either.
 
I have no idea what the Botzinger complex is (you'd better explain), and I read about the Hering breuer reflex ages ago. But as far as I remember, its purpose is to limit excessive stretching of the lungs. It doesn't cause expiration. Resting expiration is a passive process, the muscles that expanded and diminished the IPP relax, and the lung shrinks under the force of its recoil. So I don't think expiration should suffer in such a case.

If you want to increase your rate of expiration, you'd be using your accessory muscles (internal and innermost intercostals, abdominal muscles), so I don't think the vagus has a role here either.

I had written a sentence in my notes saying the Botzinger complex inhibits inspiration and promotes expiration.

Regarding the Hering breuer reflex, I just found this in West's Respiratory Physiology: The Essentials -
"The Hering-Breuer reflexes were once thought to play a major role in ventilation by determining the rate and depth of breathing. This could be done by using the information from these stretch receptors to modulate the "switching-off" mechanism in the medulla. For example, bilateral vagotomy, which removes the input of these receptors, causes slow, deep breathing in most animals. However, more recent work indicates that the reflexes are largely inactive in adult humans unless the tidal volume exceeds 1 liter, as in exercise. Transient bilateral blockade of the vagi by local anesthesia in awake humans does not change either breathing rate or volume. There is some evidence that these reflexes may be more important in newborn babies."

What I'm confused about is what the implications might be if it didn't work in newborns.
 
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