This gives a brief overview of the role of the vagal nerve in the control
of proper respiration.
Mechanical Receptors and their Effects on Respiratory Control:
Mechanical receptors located throughout the respiratory system also
contribute to the integrated control of ventilation. There are three basic
receptor classes to be considered:
1) Pulmonary Stretch Receptors
2) Irritant Receptors
3) C-fibers (small unmyelinated fibers)
Pulmonary stretch receptors:
Pulmonary stretch receptors are thought to lie within the airway smooth
muscle and are sensitive to transmural pressure gradients. These afferent
impulses travel in the vagus nerve (CN X) from the airways to the
respiratory control centers in the brainstem. The maintenance of transmural
pulmonary pressure or the release of it account for both the Hering-Breuer
reflex and the deflation reflex.
The inflation reflex (Hering-Breuer reflex) is the inhibition of inspiration
in response to an increase in transmural pulmonary pressure. It was once
thought to be an important respiratory control reflex in humans; however, we
now know that bilateral vagal blockade (temporary or permanent) does not
markedly change the respiratory rate or tidal volumes of awake humans. The
reflex can be elicited in anesthetized patients with the use of large tidal
volumes, but it is relatively unimportant in eupnic breathing. Furthermore,
patients who have undergone bilateral lung transplants have a normal rate
and depth of breathing--these lungs are completely denervated!
The deflation reflex is an increase in subsequent inspiration by a decrease
in the transmural pulmonary pressure. It too can be demonstrated in man, but
is probably not important in normal breathing. For newborns, both inflation
and deflation reflexes may play a more important role in respiratory
regulation.
Irritant receptors:
Such receptors are thought to lie between the airway epithelial cells, and
their afferent traffic is also carried in CN X. These receptors respond to a
variety of respiratory irritants such as small particles, chemicals, smoke,
and cold.
Juxtapulmonary Capillary Receptors:
Juxtapulmonary capillary receptors ("J" Receptors) are located in close
proximity to capillaries in the pulmonary interstitium. These C-fiber
afferent impulses are carried in the vagus nerve and are activated when
there is pulmonary parenchymal damage, edema formation (as in left
ventricular failure), or the release of certain chemical mediators. These
receptors have classically been thought to be responsible for the dyspnea
(shortness of breath) experienced by patients with congestive heart failure
(and subsequent pulmonary interstitial edema).
Upper Airway Receptors:
In addition to the receptors mentioned above, there are also receptors
located in the upper respiratory tract: nose, pharynx and larynx. These give
rise to reflex arcs that result in coughing or sneezing, bronchoconstriction
and tachypnea.
Gamma system of muscle control:
Many skeletal muscles contain muscle spindles which help to regulate the
tension output of the muscle. Muscle spindles have been identified (in very
small numbers) in the diaphragm, but are probably most importantly found in
intercostal muscle fibers. This feedback system helps to deliver the
appropriate amount of tension necessary for a certain mechanical load. As
the load changes, for example by a sudden increase in airway resistance or a
change in chest wall compliance, the inspiratory muscle output from the
anterior horn of the spinal cord is augmented (increased).
The major components of this feedback control system are the tension
generating muscle fibers (extrafusal m. fibers), the muscle fibers which
contain a nuclear bag structure and an annulospiral ending (intrafusal m.
fibers), a gamma efferent motor neuron fiber to the intrafusal m. fiber, an
alpha motorneuron fiber to the extrafusal m. fiber, and an afferent spindle
fiber. The major regulation occurs when there is tension on the nuclear bag.
This induces firing of the annulospiral ending which sends afferent nerve
traffic, through the dorsal root, to augment the output of the anterior horn
cells. Although this system is more complicated than presented here, the
basic plan is as follows.
The a-motorneurons are excited by descending UMNs that originate in
brainstem structures previously described, and this serves to initiate
contraction of the effector muscles (e.g., intercostal muscles). If the
tension generated is sufficient to shorten the muscle, then both the
intrafusal and extrafusal muscles shorten together, the nuclear bag is not
stretched, and there is no discharge from the annulospiral endings. If,
however, the tensions generated is insufficient to produce shortening of the
muscle, the intrafusal muscle fibers develop tension and stretching of the
nuclear bag causes discharge from the annulospiral endings. This afferent
signal is conveyed to the spinal cord via the dorsal root, and anterior horn
cell activity is increased (increased a-motorneuron output) to match the
amount of tension generated with mechanical load. In this way, the muscles
can balance their tensions output with the mechanical load.
--
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