CHAPTER 37
Regulation of Respiration 627PONTINE & VAGAL INFLUENCES
Although the rhythmic discharge of medullary neurons con-
cerned with respiration is spontaneous, it is modified by neu-
rons in the pons and afferents in the vagus from receptors in
the airways and lungs. An area known as the
pneumotaxic
center
in the medial parabrachial and Kölliker–Fuse nuclei of
the dorsolateral pons contains neurons active during inspira-
tion and neurons active during expiration. When this area is
damaged, respiration becomes slower and tidal volume great-
er, and when the vagi are also cut in anesthetized animals,
there are prolonged inspiratory spasms that resemble breath
holding (
apneusis;
section B in Figure 37–2). The normal
function of the pneumotaxic center is unknown, but it may
play a role in switching between inspiration and expiration.
Stretching of the lungs during inspiration initiates impulses
in afferent pulmonary vagal fibers. These impulses inhibit
inspiratory discharge. This is why the depth of inspiration is
increased after vagotomy (Figure 37–2) and apneusis develops
if the vagi are cut after damage to the pneumotaxic center.
Vagal feedback activity does not alter the rate of rise of the
neural activity in respiratory motor neurons (Figure 37–3).
When the activity of the inspiratory neurons is increased in
intact animals, the rate and the depth of breathing are
increased. The depth of respiration is increased because the
lungs are stretched to a greater degree before the amount of
vagal and pneumotaxic center inhibitory activity is sufficient
to overcome the more intense inspiratory neuron discharge.
The respiratory rate is increased because the after-discharge
in the vagal and possibly the pneumotaxic afferents to the
medulla is rapidly overcome.
REGULATION OF
RESPIRATORY ACTIVITY
A rise in the P
CO 2
or H
+
concentration of arterial blood or a
drop in its P
O 2
increases the level of respiratory neuron ac-
tivity in the medulla, and changes in the opposite direction
have a slight inhibitory effect. The effects of variations in
blood chemistry on ventilation are mediated via respiratory
chemoreceptors—
the carotid and aortic bodies and collec-
tions of cells in the medulla and elsewhere that are sensitive to
changes in the chemistry of the blood. They initiate impulses
that stimulate the respiratory center. Superimposed on this
basic
chemical control of respiration,
other afferents provide
non-chemical controls that affect breathing in particular situ-
ations (Table 37–1).CHEMICAL CONTROL
OF BREATHING
The chemical regulatory mechanisms adjust ventilation in
such a way that the alveolar P
CO 2
is normally held constant,
the effects of excess H
+
in the blood are combated, and the P
O 2
is raised when it falls to a potentially dangerous level. The res-
piratory minute volume is proportional to the metabolic rate,
but the link between metabolism and ventilation is CO
2
, not
O
2. The receptors in the carotid and aortic bodies are stimu-
lated by a rise in the P
CO 2
or H
- concentration of arterial
blood or a decline in its P
O 2
. After denervation of the carotid
chemoreceptors, the response to a drop in P
O 2
is abolished;
the predominant effect of hypoxia after denervation of the ca-
rotid bodies is a direct depression of the respiratory center.
The response to changes in arterial blood H
concentration in
the pH 7.3–7.5 range is also abolished, although larger changes
exert some effect. The response to changes in arterial P
CO 2
, on
the other hand, is affected only slightly; it is reduced no more
than 30–35%.
FIGURE 37–3
Afferent vagal fibers inhibit inspiratory
discharge.
Superimposed records of two breaths:
(A)
with and
(B)
without feedback vagal afferent activity from stretch receptors in the
lungs. Note that the rate of rise in phrenic nerve activity to the dia-
phragm is unaffected but the discharge is prolonged in the absence of
vagal input.
AABB012
Time (s)Summed phrenicefferent activitySummed vagalafferent activityTABLE 37–1
Stimuli affecting the respiratory center.Chemical control
CO
2
(via CSF and brain interstitial fluid H
+
concentration)
O
2
}
(via carotid and aortic bodies)
H
+Non-chemical control
Vagal afferents from receptors in the airways and lungs
Afferents from the pons, hypothalamus, and limbic system
Afferents from proprioceptors
Afferents from baroreceptors: arterial, atrial, ventricular, pulmonary