Respiratory Physiology
471
The
central chemoreceptors
are located in the medulla
and, like the peripheral chemoreceptors, provide excitatory
synaptic input to the medullary inspiratory neurons. They
are stimulated by an increase in the H
+
concentration of the
brain’s extracellular fl
uid. As we will see later, such changes
result mainly from changes in blood
P
CO
2
.
Control by P
O
2
Figure 13–34
illustrates an experiment in which healthy sub-
jects breathe low
P
O
2
gas mixtures for several minutes. The
experiment is performed in a way that keeps arterial
P
CO
2
con-
stant so that the pure effects of changing only
P
O
2
can be stud-
ied. Little increase in ventilation is observed until the oxygen
content of the inspired air is reduced enough to lower arterial
P
O
2
to 60 mmHg. Beyond this point, any further reduction in
arterial
P
O
2
causes a marked refl
ex increase in ventilation.
This refl ex is mediated by the peripheral chemorecep-
tors (
Figure 13–35
). The low arterial
P
O
2
increases the rate
at which the receptors discharge, resulting in an increased
number of action potentials traveling up the afferent nerve
fi bers and stimulating the medullary inspiratory neurons. The
resulting increase in ventilation provides more oxygen to the
alveoli and minimizes the decrease in alveolar and arterial
P
O
2
produced by the low
P
O
2
gas mixture.
It may seem surprising that we are insensitive to smaller
reductions of arterial
P
O
2
, but look again at the oxygen-
hemoglobin dissociation curve (see Figure 13–26). Total oxy-
gen transport by the blood is not really reduced very much
until the arterial
P
O
2
falls below about 60 mmHg. Therefore,
increased ventilation would not result in much more oxygen
being added to the blood until that point is reached.
To reiterate, the peripheral chemoreceptors respond to
decreases in arterial
P
O
2
, as occurs in lung disease or expo-
sure to high altitude. However, the peripheral chemoreceptors
are
not
stimulated in situations in which modest reductions
take place in the oxygen
content
of the blood but no change
occurs in arterial
P
O
2
. As stated earlier, anemia is a decrease
in the amount of hemoglobin present in the blood without a
decrease in arterial
P
O
2
, because the concentration of dissolved
oxygen in the blood is normal.
This same analysis holds true when oxygen content is
reduced moderately by the presence of carbon monoxide,
which, as described earlier, reduces the amount of oxygen com-
bined with hemoglobin by competing for these sites. Because
carbon monoxide does not affect the amount of oxygen that
can dissolve in blood, the arterial
P
O
2
is unaltered, and no
increase in peripheral chemoreceptor output occurs.
0
2
04
06
08
01
0
0
10
20
30
Normal resting level
Minute ventilation (L/min)
120
Arterial
P
O
2
(mmHg)
Figure 13–34
The effect on ventilation of breathing different oxygen mixtures.
The arterial
P
CO
2
was maintained at 40 mmHg throughout the
experiment.
Table 13–10
Major Stimuli for the Central and
Peripheral Chemoreceptors
Peripheral chemoreceptors
—carotid bodies and aortic
bodies—respond to changes in the arterial blood. They are
stimulated by:
1. Decreased
P
O
2
(hypoxia)
2. Increased hydrogen ion concentration (metabolic acidosis)
3. Increased
P
CO
2
(respiratory acidosis)
Central chemoreceptors
—located in the medulla
oblongata—respond to changes in the
brain extracellular fl
uid.
They are stimulated by increased
P
CO
2
via associated changes in
hydrogen ion concentration (see equation 13–11).
Return of alveolar and
arterial
P
O
2
toward normal
Ventilation
Respiratory muscles
Contractions
Peripheral chemoreceptors
Firing
Arterial
P
O
2
Inspired
P
O
2
Alveolar
P
O
2
Reflex via medullary
respiratory neurons
Figure 13–35
Sequence of events by which a low arterial
P
O
2
causes hyperventilation,
which maintains alveolar (and, hence, arterial)
P
O
2
at a value higher
than would exist if the ventilation had remained unchanged.
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